introduction
microbfreak@bs
Greetings!Welcome to our blog assignment!
This blog is set up for our CL1202 module - Microbiology B
Thanks for visiting and enjoy your stay here! :D
Video on the Avian Influenza virus
Sunday, February 1, 2009/ 5:31 PM
Hi! Here's some great animation! Maybe this video can help you to understand the influenza virus better.
source: http://www.youtube.com/watch?v=_yizH5FY3Ak
source: http://www.youtube.com/watch?v=_yizH5FY3Ak
Labels: Shu Juan
Picornaviridae
Before introducing this virus family to you, you need to know what pico means. Can't guess? It means very small in Greek! Yes, the virus family that I'll be introducing is Picornaviridae. It is a virus family containing the smallest viruses ever found!
Introduction:
The virus in this fammily are positive single stranded RNA viruses. They are the largest family of viruses. There are five genera in this family, the aphtovirus, cardiovirus, enterovirus, heptovirus and rhinovirus. For this time, we will be focusing on the rhinovirus, the common cold.
Rhinovirus:
The rhinovirus has naked virions without envelope. It has an isometric and symmetric nucleocapsid, although incomplete or empty capsids are relatively common. Its genomic RNA is infectious and can be used as a mRNA for direct gene transmission. It has a long untranslated region end of the 5' end structure(IRES), which is important for translation, virulence, and maybe encapsidation. Both ends of the genome is modified.As with the influenza virus, there are also 6 phases of reproduction.By using different cellular receptors, a picornavirus virion will attach to a host cell. The virion will uncoat and release the virus RNA into the cytoplasm of the host cell via a membrane channel. The virus replication occurs entirely in the cytoplasm. While the host cell's transcription processes are shut off to a degree, while the IRES helps to make sure that the virus transcription is unmodified. Replication then occurs. The RNA would be packaged into preformed capsids. The virus is then released, followed by cell lysis occurs.(with the exception of Hepatits A)
The rhinovirus infects the upper respiratory tract and has a short incubation of 2-3 days. When infection occurs, the endogenous IFN helps to defend the body. Although the locally synthesized IgA will decrease with time, the serum IgG will persist for years and recognize the virus if it enters the body again. It helps to remeber the virus!
Symptoms:
The main symptoms fpr the common cold are watery nasal discharge, congestion, sneezing, little or no fever. Sometimes, there might be fever, fatigue,cough and headache.
More Information:
The virus is tested out by virus culture, nasal washings, ELISA and PCR (polymerase chain reaction). The virus infects throughout the year and has a few serotypes circulating simultaneously. It is abundant in nasal discharge.
Control:
Since there is no vaccine for rhinovirus because there are too many rhinoviruses, the infected person should wash hands, avoid touching his or her eyes and nose, sneeze into a tissue and stay at home to prevent its spread.
www.flickr.com
Labels: Shu Juan
Orthomyxoviridae (2)
www.flickr.comSymptoms of Influenza:
Do you know that orthos means straight and myxo means mucus in Greek? That may be becuase when you're are are having a flu, you then to have a runny nose! Other than this, there are many other symptoms of flu! A person infected by the influenza virus would usually have fever, headache, body aches, fatigue, exhaustion,stuffy nose, sneezing,sore throat and cough.
www.flickr.com Lab diagnosis:
The influenza virus is detected and diagnosed by a throat gargle,swab or wash,virus culture in chick embryo, ELISA and PCR. It cannot be cultured in a nutrient media because the virus needs a live host. Influenza virus can happen throughout the year and incubates in the human boby for about 1-4 days.
Extra Information:
Sometimes antigenic shift and drift can happen. The former occurs when genes re-assort frim different subtypes and only occurs in type A influenza. The latter occurs when the genetic code of the surface antigens mutate and can happen in both influenza A and B. There are several ways to control the influenza virus, as named. The vaccine for influenza can be used, but it would not work if an antigenic shift or drift occurs, antiviral drugs, receptor analogs, transcriptase inhibitors, RT inhibitors and protease inhibitors.
The influenza virus is detected and diagnosed by a throat gargle,swab or wash,virus culture in chick embryo, ELISA and PCR. It cannot be cultured in a nutrient media because the virus needs a live host. Influenza virus can happen throughout the year and incubates in the human boby for about 1-4 days.
Extra Information:
Sometimes antigenic shift and drift can happen. The former occurs when genes re-assort frim different subtypes and only occurs in type A influenza. The latter occurs when the genetic code of the surface antigens mutate and can happen in both influenza A and B. There are several ways to control the influenza virus, as named. The vaccine for influenza can be used, but it would not work if an antigenic shift or drift occurs, antiviral drugs, receptor analogs, transcriptase inhibitors, RT inhibitors and protease inhibitors.
Labels: Shu Juan
Video on Influenza
The following video shows how humans catch a flu..
Source: http://www.youtube.com/watch?v=01qwLckBLSM
Source: http://www.youtube.com/watch?v=01qwLckBLSM
Labels: hidayah
Origins of HIV
The Origins of HIV
There are two lineages of HIV-1, both of which are related to SIV isolated from chimpanzees(cpz). Of the two lineages of HIV-1, the M lineage, is found worldwide and is responsible for the majority of human infections. The O lineage, is found only in western Africa and in France. It is not known if these two lineages represent two different introductions of HIV into humans or whether they represent a single introduction that has subsequently diverged. Very few isolations of SIV from chimps have been made, and the prevalence of SIV in chimps is not have been made, and the prevalence of SIV in chimps is not known. In fact, it has been demonstrated that SIVcpz is a natural infectious agent in wild chimp populations.
There are two lineages of HIV-1, both of which are related to SIV isolated from chimpanzees(cpz). Of the two lineages of HIV-1, the M lineage, is found worldwide and is responsible for the majority of human infections. The O lineage, is found only in western Africa and in France. It is not known if these two lineages represent two different introductions of HIV into humans or whether they represent a single introduction that has subsequently diverged. Very few isolations of SIV from chimps have been made, and the prevalence of SIV in chimps is not have been made, and the prevalence of SIV in chimps is not known. In fact, it has been demonstrated that SIVcpz is a natural infectious agent in wild chimp populations.
HIV-2 represent a distinct lineage that is closely related to SIV of sooty mangabey monkeys (smm) and of macaques (mac). SIV of African green monkeys (agm) and of mandrills (mnd) form other lineages that are more closely related to HIV-2 than to HIV-1. It is clear that SIVmm and SIVagm are naturally occurring infectious agents that are widespread in Africa and have coevolved with their monkey hosts. Sequence comparisons have shown that different isolates of SIVagm group with their hosts rather than by geography, and they are therefore adapted to their hosts. They cause no disease in their natural host, but SIVsmm does cause AIDS when transferred to Asian macaques in captivity. HIV-2 is found primarily in western central Africa, where its distribution is almost coincident with that of mangabey monkeys. It seems clear that HIV-2 represents a separate introduction of SIV from a different monkey host into humans.
Thus, SIV must be the source of HIV, with different viruses serving as the source of HIV-1 and HIV-2. When the viruses crossed the species barrier and became established in man as HIV is not clear. HIV-1 has been isolated from serum collected in 1959 in Zaire and antibodies to HIV have been found in serum collected in 1963 in Burkino-Faso, so HIV-1 has been in the human population at least that long. From sequencing studies of the glycoprotein gene and examination of the rate of divergence, one estimate is that the virus might have entered the human population about 70 years ago, although estimates of divergence rates are controversial. A likely scenario is that the viruses have been introduced into human populations many times in the past but failed to become epidemic. Infections in humans either died out because of the low transmissibility of the virus or smoldered in only a small fraction of the population. The different lineages of HIV-1 and, especially, of HIV-2 suggest, in fact, that they may result from independent introductions into humans, consistent with the hypothesis that multiple introductions of both viruses have occurred.
Recent changes in human behaviour, including more extensive travel by truck, bus, and plane, changes in sexual practices, and the use of injectable drugs, as well as the increase in the human populations, could have allowed the virus to spread more extensively than in the past and to become epidemic worldwide. The spread of the virus could also have been aided by the appearance of mutants that were more easily transmissible from person to person. The large increase in population during the last century has certainly resulted in more opportunities for the introduction and spread of the virus in humans, and therefore for the selection of such transmissible mutants.
Labels: Natasya
Flavivirus
All viruses in the flavivirus family are single-stranded RNA with linear non-segmented genome.Viruses in this family are considered positive (+) sense because proteins are made directly from the template strand of RNA which is present in the viral capsid.
After being bitten by a mosquito carrying the virus, the incubation period ranges from three to 15 days before the signs and symptoms of dengue appear. Dengue starts with chills, headache, pain upon moving the eyes, and low backache. Painful aching in the legs and joints occurs during the first hours of illness. The temperature rises quickly as high as 40° C, with relative low heart rate and low blood pressure. The eyes become reddened. A flushing or pale pink rash comes over the face and then disappears. The glands (lymph nodes) in the neck and groin are often swollen.
Fever and other signs of dengue last for two to four days, followed by rapid drop in temperature with profuse sweating. This precedes a period with normal temperature and a sense of well-being that lasts about a day. A second rapid rise in temperature follows. A characteristic rash appears along with the fever and spreads from the extremities to cover the entire body except the face. The palms and soles may be bright red and swollen.
Viruses in Flavi genera are transmitted by arthropods, mainly mosquitoes and ticks. Flaviviruses that are transmitted by arthropods are known as Group B Arboviruses. Arboviruses include Dengue fever,yellow fever and west nile.
Major diseases caused by the Flaviviridae family include:
- Dengue Fever
- Dengue Fever
- Yellow Fever
- West nile Encephalitis
Dengue Fever
Dengue fever is the most common flavivirus infection among humans. The incidence of disease corresponds to the worldwide dispersion of the principal vector, A aegypti, which serves to maintain the virus in a human-mosquito-human cycle.Epidemiologic patterns are highly varied but may be described as epidemic, endemic, or hyperendemic. In endemic regions, dengue fever occurs principally in children and often is unrecognized. In Southeast Asia where all four serotypes are continuously transmitted, epidemics of dengue hemorrhagic fever are a major cause of death among children, involving thousands of cases and a 3 to 10 percent case fatality rate.
After being bitten by a mosquito carrying the virus, the incubation period ranges from three to 15 days before the signs and symptoms of dengue appear. Dengue starts with chills, headache, pain upon moving the eyes, and low backache. Painful aching in the legs and joints occurs during the first hours of illness. The temperature rises quickly as high as 40° C, with relative low heart rate and low blood pressure. The eyes become reddened. A flushing or pale pink rash comes over the face and then disappears. The glands (lymph nodes) in the neck and groin are often swollen.
Fever and other signs of dengue last for two to four days, followed by rapid drop in temperature with profuse sweating. This precedes a period with normal temperature and a sense of well-being that lasts about a day. A second rapid rise in temperature follows. A characteristic rash appears along with the fever and spreads from the extremities to cover the entire body except the face. The palms and soles may be bright red and swollen.
Because dengue is caused by a virus, there is no specific medicine or antibiotic to treat it. For typical dengue, the treatment is purely concerned with relief of the symptoms. Rest and fluid intake for adequate hydration is important.
Yellow Fever
Yellow Fever is caused by a virus and spread to humans by the bite of an infected mosquito. The virus causes sudden onset of fever, four days after the bite. Most cases are mild, last less than a week, and the person makes a full recovery. Sometimes it is more serious. The liver may be damaged leading to jaundice - a yellowish tinge to the skin. Hence the name 'yellow' fever. It may cause joint pain and vomiting.
The initial or "acute" phase is normally characterized by high fever, general muscle pain, backache, shivers, headache, loss of appetite, nausea, and vomiting. Most patients improve and their symptoms disappear after three to four days. About 15 percent of those infected enter a "toxic" phase. In this phase, high fever reappears and can lead to shock, bleeding (from mouth, nose, eyes, and/or stomach), and kidney and liver failure.
Liver failure causes jaundice (yellowing of the skin and the whites of the eyes), which gives yellow fever its name. About half of the patients in the toxic phase die within 10 to 14 days. Persons recovering from yellow fever have lifelong immunity against reinfection.
West nile Encephalitis
West Nile virus is a mosquito-borne virus that can cause encephalitis (inflammation of the brain) or meningitis (inflammation of the lining of the brain and spinal cord). It is to humans by the bite of an infected mosquito. A mosquito becomes infected by biting a bird which carries the virus. West Nile virus is not transmited by person-to-person contact such as touching, kissing, or caring for someone who is infected.
Most people who were infected with the West Nile virus had no symptoms or experienced mild illness with fever, headache and body aches before fully recovering. some people also developed a mild rash or swollen lymph glands. In some individuals, particularly the elderly, West Nile virus can cause serious disease that affects brain tissue. At its most serious, it can cause permanent neurological damage and can be fatal. Encephalitis (inflammation of the brain) symptoms include the rapid onset of severe headache, high fever, stiff neck, confusion, loss of consciousness, and muscle weakness. Death may occur in some instances.
There is no specific treatment for West Nile encephalitis other than supportive therapy for severe cases. Antibiotics will not work because a virus, not bacteria, causes West Nile disease. Currently no vaccine for the virus is currently available
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Prevention & Treatment For AIDS
Prevention and Treatment of AIDS
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The most successful method for the prevention of most viral disease has been the development of vaccines. However, the development of a vaccine against HIV has been a very slow, frustrating, and to date unsuccessful process. This is perhaps not surprising in light of the fact that the virus establishes a persistent lifelong infection in the face of a vigorous immune response on the part of the host that succeeds in controlling the virus for many years. Vaccine development continues to be a priority, but to the current time only public education to slow the spread of the disease and the development of antiviral drugs have had any success in control of the virus.
Much effort has been made to reduce the epidemic spread of HIV by educating the public and thereby altering patterns of behaviour, especially sexual behaviour. AIDS is a significant health problem in the United States, particularly in urban areas, and has become one of the major causes of death for persons in their most productive years. However, safe sex practices, such as the use of condoms, have lowered the numbers of now infections, especially for HIV infections among gay white men. Education campaigns in Thailand and Uganda have succeeded in slowing the spread of the disease, and similar campaigns in other areas of the world have met with at least some success. However, although such campaigns slow the spread of the virus, they do not stop it and will never succeed in eliminating the virus from the population.
Although this therapy has been successful in many patients, it is clearly not a panacea. First, it is very expensive and suitable for use only in developed countries that can afford a very high level of health care. Second, it requires taking dozens of pills a day at precisely timed intervals, and compliance becomes a major issue when the therapy must be continued indefinitely. It may be for this reason that the therapy fails in a significant fraction of HIV patients. However, although this treatment is quite complex and of limited success, its very existence seemingly has led to a rise in unprotected sexual activity and to an upsurge in the rate of HIV infection among populations at risk.
Attempts to develop a vaccine continue and there is hope that a vaccine may ultimately be produced. It is clear that an immune response that involves both neutralizing antibodies and CD8+ T cells is important in the control of the virus during the clinically latent state. The T-cell response seems to be especially important. Stronger CTL responses result in lower levels of virus production during the latent state, which results in a slower rate of progression to AIDS. Neutralizing antibodies are also important, but it has been found that fresh isolates of virus from patients are difficult to neutralize, presumably because of the many carbohydrate chains attached to the HIV surface glycoprotein and because of the unusual folding properties of this protein. In addition, variants arise during prolonged infection that are resistant to the mix of antibodies that exist in the patient at the time that the variants arise.
The possibility of a live virus vaccine is suggested by the finding that a small fraction of infected people exists who have not progressed to AIDS after 10-15 years of infection and whose CD4+ T-cell count has remained fairly stable. In at least some of these individuals, the infecting HIV strain has deletions in nef. Intriguingly, experiments with nef deletions in SIV in monkeys give comparable results – the monkeys do not develop AIDS and they are protected from infection by wild-type strains of SIV. However, any attempt to develop a live virus vaccine for a virus that establishes a persistent infection that is ultimately fatal, and for which the symptom of disease are delayed for many years, faces formidable obstacles.
Labels: Natasya
Spread of AIDS
Spread of AIDS
HIV is spread sexually, through contaminated blood, and from mother to child. The virus is present in semen, both as free virus and in infected cells, and in vaginal secretions of infected people, and can be transmitted by either homosexual or heterosexual intercourse. The probability of a woman becoming infected during unprotected vaginal intercourse with an infected male is estimated at less than 1/50. The risk of a man becoming infected during heterosexual intercourse is less. The risk is much higher if genital lesions resulting from sexually transmitted diseases are present. The risk of infection is also much higher during receptive anal intercourse. The use of condoms reduces the risk of transmission considerably.
The virus can also be spread by means of contaminated blood, whether through blood transfusions, the use of contaminated products by haemophiliacs, by needle stick in health care workers, the sharing of needles by injecting drug users, or via tattoo needles. Blood transfusion was an important source of infection before the development of test for the virus and remains a problem in developing countries where blood tests may not be regularly available. Similarly, many hemophiliacs became infected before the development of blood tests. Use of blood tests and screening of donors for risk factors have greatly reduced the risk of transmission of HIV through blood products in developed countries. However, transmission among drug users remains an important source of infection.
Untreated, infected women transmit the virus to a newborn child about one-fourth of the time. Transmission can occur during delivery or during breast feeding. The use of anti-HIV drugs has reduced transmission to infants in countries where the drugs are available.
At the end of 1999, an estimated 43 million people were living with HIV/AIDS, with about 1 million of those in North America. The cumulative death toll from AIDS since the beginning of the epidemic reached 20 million in the first half of 2000. More than 5 million new infections occurred worldwide in 1999, and about 5.4 million people died of AIDS that year. In the absence of treatment, virtually all infected people go on to develop AIDS and die within 2 years of the appearance of the symptoms of AIDS.
At the end of 1999, an estimated 43 million people were living with HIV/AIDS, with about 1 million of those in North America. The cumulative death toll from AIDS since the beginning of the epidemic reached 20 million in the first half of 2000. More than 5 million new infections occurred worldwide in 1999, and about 5.4 million people died of AIDS that year. In the absence of treatment, virtually all infected people go on to develop AIDS and die within 2 years of the appearance of the symptoms of AIDS.
The focus of HIV infection is sub-Saharan African, where25 million people, or more than 5% of the population, are thought to be infected and where medical care is still primitive. In the 15 years from 1984 to 1999, the number of HIV infections increased dramatically. The extent of the problem is illustrated by the fact that in some large cities in sub-Sahara Africa, an estimated 20-40% of adults may be infected. The spread of HIV has resulted in a marked decrease in life expectancy, which has reversed a long period of increasing life expectancy as health care standards have improved. In other areas of the world, HIV continues to spread but has not reached the extreme levels found in parts of Africa.
In Latin America and in southern and southeast Asia, about 0.6% of the population is infected. In North America, western Europe, and Australia, estimates are that 0.3% of the population is infected. In North America, HIV has been spread primarily through homosexual contacts and by sharing needles by drug users who inject drugs, but the frequency of heterosexual transmission is increasing. In developing countries, heterosexual contact is the primary mode of transmission.
In the United States, the number of newly diagnosed cases of AIDS, especially in white homosexual men, has dropped because awareness of the disease has led to the more frequent use of condoms and a lowered incidence of multiple sex partners, and because more effective drug therapies have been introduced.
Labels: Natasya
serological methods
Serological tests may be performed for diagnostic purposes when an infection is suspected.
There are several serology techniques that can be used depending on the antibodies being studied. These include: ELISA, Haemagglutination Inhibition Test and Complement Fixation.
ELISA
Enzyme-linked Immunosorbent Assay (ELISA) is a biochemical technique used mainly in immunology to detect the presence of an antibody or antigen in a sample. In simple terms, in ELISA an unknown amount of antigen is affixed to a surface, and then a specific antibody is washed over the surface so that it can bind to the antigen. This antibody is linked to an enzyme, and in the final step a substance is added that the enzyme can convert to some detectable signal.
The diagram below shows two different types of ELISA.
Hemagglutination Inhibition Test (HI)
Hemagglutination inibition assay is a clinical lab test used to detect the presence of a a certain hemagglutinating virus or other hemagglutinin antigen based on whether the red blood cells in the sample lose the ability to clump together when the antibody to the virus or other antigen is added to it. If the virus or antigen is present, the antibody kills it and thereby stops it from being able to stick the red blood cells to each other.
The direct measurement of antibody binding to antigen is used in most quantitative serological assays. However, some important assays are based on the ability of antibody binding to alter the physical state of the antigen it binds to. These secondary interactions can be detected in a variety of ways. For instance, when the antigen is displayed on the surface of a large particle such as a bacterium, antibodies can cause the bacteria to clump or agglutinate. The same principle applies to the reactions used in blood typing, only here the target antigens are on the surface of red blood cells and the clumping reaction caused by antibodies against them is called hemagglutination
Complement Fixation
The complement fixation test is based on the use of complement, a biological substance present in the sera of normal animals. Its great value is its predictable activity in the presence of serologically reacting factors and its nonspecificity, that is, it is not like an antibody with a narrow range of reactions or increased concentration occurring in a host following immunization or infection. Furthermore, it is easily destroyed by heating at temperatures that have no deleterious effect on antibodies
It is the nature of complement not to react with an antigen or an antibody alone but to enter into combination with antigen-antibody complexes. The lack of specificity of complement allows it to react with almost any antigen-antibody complex. Therefore, in this test procedure, unless complement is fixed by the particular antigen and antibody system in question, it will remain free to react as an indicator, resulting in a "negative" test. If on the other hand, complement is fixed by the antigen and antibody system under study, it is not free to react in the indicator system, resulting in a "positive" test. The indicator system used in CF is sheep red blood cells (RBCs). In a positive or reactive test, the complement is bound to an antigen-antibody complex, and is not free to interact with sensitized RBCs so they remain unlysed and settle to the bottom of the well to form a button. On the other hand, in a negative or nonreactive test, the complement remains free since there is no antigen-antibody complex for it to bind to, and it interacts with the sensitized RBCs causing them to lyse.
Labels: nadiah
AIDS The Disease
AIDS, the Disease
With time the immune system is overwhelmed, with the result that the replication of HIV escalates, opportunistic fungal, protozoal, bacterial, and viral infection occur, characteristic cancers appear, and neurological symptoms become apparent. The time to progression to AIDS following infection by HIV is variable but average about 10 years.
Symptoms occur much sooner in infants infected at birth, perhaps because the immune system is not as well developed. In adults infected by the virus, the time to appearance of the symptoms of AIDS is correlated with the level of viral replication during the latent period. In individual in which viral replication is high, the CD4+ T-cell count declines faster and the time to appearance of AIDS is shorter. The rate of virus replication is probably a function of the strength of the immune response against the virus, especially the CD8+ CTL response. Individuals with a better immune response control virus replication better and longer. Once the symptoms of AIDS appear, the time to death is usually 1-2 years unless antiviral treatment is administered.
CD4+ T cells, most of which function as T helper cells, are a critical part of the immune system. They are necessary for an immune response to an antigen, whether the response is to produce CD8+ CTLs or to produce circulating antibodies. AIDS results when so few CD4+ t cells are present that the body is unable to mount an effective immune response. The first symptoms usually occur when the CD4 T-cell concentration falls below 500/ul and may include reactivation of viruses such as Herpes Zoster, reactivation of bacteria such as Mycobacteria tuberculosis, oral lesions caused by fungi, or lymph node pathology. These first symptoms are sometimes referred to as AIDS-related complex or ARC. Full-blown AIDS is normally signalled by a drop in the CD4+ T-cell concentration below 200/ul. At this point the infected individual becomes susceptible to numerous opportunistic infections, including those of microorganisms such as Pneumocystis carinii, bacteria such as Mycobacterium, and fungi such as yeast.
Viruses that are normally controlled by the immune system become a problem, such as cytomegalovirus and Herpes Simplex virus. Several virus-induced cancers become common, such as lymphoma caused by Epstein-Barr virus, Kaposi’s sarcoma caused by human Herpesvirus-8, or anogenital carcinoma caused by Human Papilloma virus. Many of these opportunistic diseases, such as P. Carinii pneumonia or Kaposi’s sarcoma, are rarely seen in non-HIV-infected people. Others are regularly seen in the general population but HIV-infected individuals have a much higher incidence of the disease, 100-fold higher in the case of lymphoma, for example. Other symptoms of AIDS include a wasting syndrome and neurological abnormalities, described below. The symptoms of AIDS become progressively worse as the CD4+ count continues to drop until virtually no CD4+ cells are present. The decline in numbers of CD4+ cells is accelerated by the increased replication of HIV during this terminal phase, when the immune system can no longer control viral infection.
The lymph nodes are organs that trap invading pathogens and present them to immune cells. Large numbers of macrophages and CD4+ T cells are present in lymph nodes, and the nodes are sites of active HIV replication. During the progression of disease following HIV infection, the lymph nodes deteriorate. During the final stages of disease, the architecture of the nodes is completely destroyed and this loss of lymph node function contributions to the loss of immune function.
A wasting syndrome is characteristic of late-stage HIV infection. Bowel involvement results in diarrhea and malabsorption. The wasting syndrome is thought to be a symptom of HIV infection itself, but opportunistic infections of the gut probably the symptoms in many individuals.
Most HIV-infected individuals suffer, sooner or later, from neurological disease. Some disease is caused by opportunistic pathogens, such as progressive multifocal leukoencephalopathy caused by JC virus. However, two-thirds of infected individuals develop an encephalopathy induced by HIV infection itself that produces symptoms including dementia, motor and behavioural abnormalities, and seizures. These symptoms are referred to as AIDS dementia complex. HIV is present in the brains of infected individuals in macrophages and microglia, but does not infect neurons. The cause of the neuronal loss induced by HIV infection is unknown.
Labels: Natasya
HIV
Human Immunodeficiency Virus
The two human Lentiviruses, HIV-1 and HIV-2, cause the well-known disease called AIDS (Acquired Immunodeficiency Syndrome). Although both HIV-1 and HIV-2 cause AIDS in people, HIV-2 is not as serious a pathogen. The latent period before disease develops is longer, the virus is not as easily transmissible, and it has not spread as extensively as has HIV-1. It is HIV-1 that is responsible for the vast majority of AIDS in people, and HIV-1 has correspondingly been much more exhaustively studied.
The primary cellular targets of HIV in infected humans are macrophages and CD4+ T cells. These cells express CD4, the primary receptor for all primate Lentiviruses, as well as chemokine coreceptors that are also required for entry of the virus.The infection of macrophages and of CD4+ T cells differs in several important respects. HIV can replicate in fully differentiated, non-dividing macrophages, but infection of macrophages does not lead to extension cytopthology. Efficient infection of CD4+ T cells, in contrast, require that the T cell be activated and results in the death of the cell. Strains of HIV are known that infect macrophages (M-tropic virus) or T cells (T-tropic) more efficiently, which is a function of the env gene of the virus.
Primary infection may be asymptomatic (most infected people do not see a doctor on primary infection) or accompanied by nonspecific symptoms that appear 3-6 weeks after infection. Symptoms may include rash, fever, diarrhea, arthralgia, myalgia, nausea, sore throat, lethargy, headache, or stiff neck. The number of CD4+ T cells declines during this phase. An immune response is mounted that includes both CD8+ cytotoxic T cells (CTLs) and antibody production. This reduces the amount of virus in the blood, the number of CD4+ T cells recovers but does not reach preinfection levels, and symptoms of disease ameliorate. However, clearance of the virus is not complete, and a long period of clinical latency ensues. During this period, even though the infected individual is often asymptomatic, the virus continues to replicate actively, especially in lymph nodes, and the immune system continues to fight the infection. It has been estimated that during this clinically quiescent period 10^8 to 10^9 virus particles per day are released into the peripheral blood supply (and cleared). During this time the turnover of CD4+ lymphocytes is also 10^8 to 10^9 cells per day.
In untreated individuals, the continuing replication of virus results in a steady decline in the number of CD4+ T cells and the continuing appearance of mutations in the virus. In the Env protein, the rate of change in the amino acid sequence average about 2.5% per year, with a large fraction of changes occurring in certain hyper-variable regions. It seems clear that this accumulation of mutations is driven, at least in part, by immune selection.
Labels: Natasya
Lentivirus
Saturday, January 31, 2009/ 11:47 PM
Lentiviruses
The Lentiviruses are complex Retroviruses whose core is cone shaped in the mature virion. The most important are the Human Immunodeficiency Viruses, HIV-1 and HIV-2. Other members of the genus include Simian Immunodeficiency Virus (SIV), Feline Immunodeficiency Virus (FIV), Bovine Ficiency Virus (BIV), Visna virus (which causes disease in sheep), Equine Infectious Anemia virus (EIAV), and Caprine Arthritis-Encephalitis Virus (CAEV). As described above, the regulation of Lentivirus replication is complex because Lentiviruses encode three to six accessory genes, depending on the virus, to regulate the replication cycle and aid in the assembly of progeny viruses.
All Lentiviruses have a specific tropism for macrophages, which comprise the major reservoir of infected cells in an animal. Other cells can also be infected and this can be important in the disease process (e.g., CD4+ T cells in HIV infection). Lentiviruses establish a lifelong, chronic infection which elicits a vigorous immune response that is still unable to clear the infection. Most known Lentiviruses cause serious disease in their native host after a long latent period. However, SIV produces a asymptomatic, lifelong infection of its natural host, African monkeys. Intriguingly, SIV causes AIDS when transmitted to Asian monkeys.
Labels: Natasya
Integration
Integration (Retrovirus)
After the appearance of the full-length dsDNA genome in the nucleus, the viral integrase catalyzes it insertion into a host cell chromosome by means of a single recombinational event. Insertion is essentially random within the host genome. The first event in integration is the removal of two nucleotides from the 3’ end of both strands of the viral DNA. The next two nucleotides are always AC, from 3’ to 5’. The 3’ OH of the now 3’-terminal A residue is used to attack an internucleotide phosphate in the host DNA. Attack is coordinated so that both ends of the viral DNA are inserted at once. The spacing between the two insertion points depends on the viral integrase and is 4, 5, or 6 nucleotides in different viruses. The ends of the inserted structure are then cleaned up, probably by host enzymes. Insertion results in the loss of the two terminal nucleotides of the viral DNA. In addition, a duplication of the 4, 5, or 6 nucleotides of the host that lie between the two insertion points is produced, and these duplicated nucleotides flank the two ends of the viral genome.
The integrated form of the virus, the provirus, is stable. No mechanism for precise excision of the provirus is known, and integration is essentially irreversible. Most Retroviruses do not kill the host cell, and the provirus behaves as a simple Mendelian gene that is transmitted to all daughter cells. It is obvious that insertion of such a provirus into the germ line would lead to its transfer to progeny organisms, which appears to have occurred many times in the past.
After the appearance of the full-length dsDNA genome in the nucleus, the viral integrase catalyzes it insertion into a host cell chromosome by means of a single recombinational event. Insertion is essentially random within the host genome. The first event in integration is the removal of two nucleotides from the 3’ end of both strands of the viral DNA. The next two nucleotides are always AC, from 3’ to 5’. The 3’ OH of the now 3’-terminal A residue is used to attack an internucleotide phosphate in the host DNA. Attack is coordinated so that both ends of the viral DNA are inserted at once. The spacing between the two insertion points depends on the viral integrase and is 4, 5, or 6 nucleotides in different viruses. The ends of the inserted structure are then cleaned up, probably by host enzymes. Insertion results in the loss of the two terminal nucleotides of the viral DNA. In addition, a duplication of the 4, 5, or 6 nucleotides of the host that lie between the two insertion points is produced, and these duplicated nucleotides flank the two ends of the viral genome.
The integrated form of the virus, the provirus, is stable. No mechanism for precise excision of the provirus is known, and integration is essentially irreversible. Most Retroviruses do not kill the host cell, and the provirus behaves as a simple Mendelian gene that is transmitted to all daughter cells. It is obvious that insertion of such a provirus into the germ line would lead to its transfer to progeny organisms, which appears to have occurred many times in the past.
Labels: Natasya
Why is Genome Diploid?
Why Is the Genome Diploid?
Why the retroviral genome is not clear. In other instances where reverse transcription occurs, such as in the Hepadnaviruses and the Retrotransposons, the RNA to be copied is not diploid. Furthermore, in vitro studies have shown that retroviral RT can use a single copy of the RNA genome to produce a full-length dsDNA. Thus, two copies of the genome are not essential. However, it is possible that during infection the process is more efficient if the RT can go back and forth between the two copies, and this resulted in selection for a diploid genome in Retroviruses. The process of reverse transcription to produce the viral dsDNA is complex with the multiple jumps more efficient. Other possible advantages of a diploid genome that could have resulted in selective pressure for diploid are the possibility of overcoming at least some damage in the RNA by switching templates, and the fact that switching templates result in recombination. Recombination does occur frequently in Retroviruses, and it is clear from many studies of virus evolution that recombination is important in their evolution.
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Synthesis of 2nd DNA Strand (RETROVIRUS)
Synthesis of the Second DNA Strand
The first-strand DNA produced in this way is the template for second-strand (plus-strand) DNA synthesis. The primer for second-strand is an RNA oligonucleotide, called the polypurine tract or PPT, positioned immediately 5’ of U3, PPT survives RNase H degradation and its 3’ terminus is exact; that is, the cleavages to produce it are precise. In addition to this precise primer for plus-strand synthesis, which defines the boundary of U3 and thus of the LTR, additional priming sites are used in some Retroviruses, such as HIV.
The PPT plus-strand primer is extended through U3, R, U5, and into the region of the primer tRNA, which is still attached to the first-strand DNA. The 18 nucleotides of the tRNA primer that are complementary to the PBS are copied, but further copying is thought to be blocked by a modified nucleotide in the tRNA that cannot be copied. The tRNA primer is then removed by RNase H and a second jump occurs. In the second jump, the nascent second-strand DNA is transferred to the other end of the template, using the PBS sequence, which is now present at the 3’ ends of both strands. Synthesis of both strands of DNA resumes and it becomes full length and double stranded. The resulting dsDNA is cleaned up, probably by cellular enzymes. In the full-length, linear ds copy of the genome, the LTR sequence U3-R-U5 has been formed at both ends of the DNA genome.
It is of interest that RT, like DNA polymerases, requires a primer to synthesize DNA, but unlike most DNA polymerases it can copy either DNA or RNA, given the appropriate primers. Thus, the enzyme differs from the RNA replicases of RNA viruses, which use other mechanisms for the initiation of RNA replication.
The first-strand DNA produced in this way is the template for second-strand (plus-strand) DNA synthesis. The primer for second-strand is an RNA oligonucleotide, called the polypurine tract or PPT, positioned immediately 5’ of U3, PPT survives RNase H degradation and its 3’ terminus is exact; that is, the cleavages to produce it are precise. In addition to this precise primer for plus-strand synthesis, which defines the boundary of U3 and thus of the LTR, additional priming sites are used in some Retroviruses, such as HIV.
The PPT plus-strand primer is extended through U3, R, U5, and into the region of the primer tRNA, which is still attached to the first-strand DNA. The 18 nucleotides of the tRNA primer that are complementary to the PBS are copied, but further copying is thought to be blocked by a modified nucleotide in the tRNA that cannot be copied. The tRNA primer is then removed by RNase H and a second jump occurs. In the second jump, the nascent second-strand DNA is transferred to the other end of the template, using the PBS sequence, which is now present at the 3’ ends of both strands. Synthesis of both strands of DNA resumes and it becomes full length and double stranded. The resulting dsDNA is cleaned up, probably by cellular enzymes. In the full-length, linear ds copy of the genome, the LTR sequence U3-R-U5 has been formed at both ends of the DNA genome.
It is of interest that RT, like DNA polymerases, requires a primer to synthesize DNA, but unlike most DNA polymerases it can copy either DNA or RNA, given the appropriate primers. Thus, the enzyme differs from the RNA replicases of RNA viruses, which use other mechanisms for the initiation of RNA replication.
Labels: Natasya
Orthomyxoviridae (1)
www.flickr.comIntroduction:
For this family of viruses, we'll be focusing on the Influenza virus (type A and B). The influenza virus is a single stranded negative RNA (ss(-) RNA) virus. An influenza virus particle is typically spherical, has an envelope, could be pleomorphic,has spikes on the envelope called haemagglutinin and neuraminidase,the ratio of HA:NA is 5:1.
As mentioned earlier, the virus is a ss(-) RNA in 8 segments. It has 3 polymerase polypeptides with each segment and the 5' and 3' end of the segments are all highly conserved.
Reproductive cycle of the Influenza virus:
There are basically 6 phases for virus replication. They are:
- Attachment
- Penetration
- Uncoating
- Replication
- Assembly
- Release
It takes about 6 hours for the complete replication of the Influenza virus. The reproduction of the virus kills the host cell in process. The virus attaches to the glycolipids or glycoproteins of the cell membrane of the host cell via its haemugglutinin subunit on the virion envelope. Then, the virus is engulfed into the endosomes. The acidic environment of the endosome causes the virus envelope to fuse with the endosome's plasma membrane, and in the process, uncoating the nucleocapsid which is released into the cytoplasm. A transmembrane protein help forms an ion channel for protons to enter the virion and destabilize protein binding. This allows the transport of the nucleocaspid to the nucleus, where the genome is transcribed by important enzymes to get viral mRNA. The nucleocaspid is then assembled in the nucleus. As the virions bud through the host cell membranes, they acquire envelopes and undergo maturation. The viral envelope haemagglutinin may be subjected to degradation(digestion). This process helps the virions to be infectious. Virions that are newly synthesized have surface glycoproteins that contain a N-acetylneuraminic acid as a part of their carbohydrate structure.This factor makes them susceptible to self-agglutination by the hemagglutinin. One of the functions of the viral neuraminidase is to remove these residues, to avoid self-agglutination.
Pathogenesis:
The influenza virus is transmitted from person to person in droplets mostly by sneezing and coughing. The inhaled droplets then land on the lower espiratory tract and the virus starts to invade and infect the mucosal cells. The influenza virus affects the human respiratory tract because of its haemagglutinin's (HA) affinity for receptors in the epithelium of the tract. In an attempt to fight off the virus, the epithelium of the tract produces mucus to trap the virus particles. The virus may extensively infect the alveoli, especially pateints who have lung and heart problems. Some of the compounds that help to fight off these virus are:
- existing antibodies
- Macrophages
- IgA, IgG
- Anti-HA Ab
- Cytokines www.humpath.com
- Natural killer cells
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Synthesis of 1st DNA Strand (RETROVIRUS)
Synthesis of First DNA Strand
At the ends of the viral RNA are domains that are essential for production of the dsDNA copy of the RNA genome. A direct repeat element called R, 15-230 nt in length depending on the virus, is present at the two ends of the RNA genome. At the 5’ end of the genome, a unique sequence element called U5 (70-220 nt long) is present immediately downstream of R, and at the 3’ end of the genome a unique element called U3 (230-1200 nt) is present immediately upstream of R. On completion of DNA synthesis, these elements give rise to direct repeats present at the ends of the viral DNA, called the long terminal repeats or LTRs, which have the sequence U3—U5.
Immediately 3’ of U5 is a primer binding site (PBS), where 18 nucleotides are exactly complementary to the 3’ end of a specific cellular tRNA. Each genomic RNA molecule has bound to it at PBS one molecule of the appropriate tRNA, which is used as a primer for DNA synthesis. The tRNA used depends on the virus, and several different tRNAs are known to be used by different viruses.
Reverse transcription begins by extending the primer tRNA through U5 and R, and stops when the end of the RNA genome is reached. The cDNA product, called the first strong stop DNA, is then transferred while still attached to the primer, from the 5’ end of the RNA to the 3’. It is unknown whether transfer is usually to the 3’ end of the same molecule, to the 3’ end of the second copy of the genome, or randomly to either copy of the RNA in the virus. This transfer uses the repeat element R at the 5’ end 3’ ends – the DNA copy detaches from R at the 5’ end and anneals to R at the 3’ end, so that only one copy of R is present in the DNA transcript. RNase H is presumably important for this. During reverse transcription, the RNA strand is destroyed by RNase H about 18 nt behind the transcription point. The degradation of the RNA strand during transcription of the DNA copy may encourage the jump to the other end. Other components of the particle may also be involved in the jump.
After the jump, reverse transcription resumes until the 5’ end of the RNA template is reached. Note that the RNA strand now at PBS because RNase H has degraded the RNA strand of the DNA/RNA hybrid (but not the RNA in PBS because this is an RNA-RNA duplex). This process results in the formation of what is called first-strand DNA or minus-strand DNA, because it is the antimessage sense.
At the ends of the viral RNA are domains that are essential for production of the dsDNA copy of the RNA genome. A direct repeat element called R, 15-230 nt in length depending on the virus, is present at the two ends of the RNA genome. At the 5’ end of the genome, a unique sequence element called U5 (70-220 nt long) is present immediately downstream of R, and at the 3’ end of the genome a unique element called U3 (230-1200 nt) is present immediately upstream of R. On completion of DNA synthesis, these elements give rise to direct repeats present at the ends of the viral DNA, called the long terminal repeats or LTRs, which have the sequence U3—U5.
Immediately 3’ of U5 is a primer binding site (PBS), where 18 nucleotides are exactly complementary to the 3’ end of a specific cellular tRNA. Each genomic RNA molecule has bound to it at PBS one molecule of the appropriate tRNA, which is used as a primer for DNA synthesis. The tRNA used depends on the virus, and several different tRNAs are known to be used by different viruses.
Reverse transcription begins by extending the primer tRNA through U5 and R, and stops when the end of the RNA genome is reached. The cDNA product, called the first strong stop DNA, is then transferred while still attached to the primer, from the 5’ end of the RNA to the 3’. It is unknown whether transfer is usually to the 3’ end of the same molecule, to the 3’ end of the second copy of the genome, or randomly to either copy of the RNA in the virus. This transfer uses the repeat element R at the 5’ end 3’ ends – the DNA copy detaches from R at the 5’ end and anneals to R at the 3’ end, so that only one copy of R is present in the DNA transcript. RNase H is presumably important for this. During reverse transcription, the RNA strand is destroyed by RNase H about 18 nt behind the transcription point. The degradation of the RNA strand during transcription of the DNA copy may encourage the jump to the other end. Other components of the particle may also be involved in the jump.
After the jump, reverse transcription resumes until the 5’ end of the RNA template is reached. Note that the RNA strand now at PBS because RNase H has degraded the RNA strand of the DNA/RNA hybrid (but not the RNA in PBS because this is an RNA-RNA duplex). This process results in the formation of what is called first-strand DNA or minus-strand DNA, because it is the antimessage sense.
Labels: Natasya
Reverse Transcription of Viral RNA
Most Retroviruses penetrate into a cell by fusion with the plasma membrane, but some use the endosomal pathway. Once inside the cell, reverse transcription takes place in a subviral particle to produce a full-length, linear dsDNA copy of the RNA. The composition of this subviral particle is not well defined. It certainly contains RT and its associated activities as well as components derived from Gag, but which Gag components are present and whether cellular proteins form part of this particle are not known.
Reverse transcription begins in the cytoplasm. In most viruses, the full-length dsDNA is produced in the cytoplasm, but in some the finishing touches occur after transfer to the nucleus. After transfer to the nucleus, the viral DNA is integrated into the host chromosome, essentially t random, in a process that requires the activity of IN. In the simple viruses, transfer to the nucleus occurs during cell division, when the nuclear envelope is disassembled. At least some of the complex retroviruses, however, such as HIV, encode proteins that allow the DNA-containing complex to traverse the nuclear membrane. Thus, the simple Retroviruses can only productively infect dividing cells, whereas HIV can infect non-dividing cells.
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Retroviral Genome
The RNA genome in the retrovirion is diploid, consisting of two copies of a 7- to 10-kb single-stranded (ss) RNA that is capped and polyadenylated. The two copies of the genome are normally identical, but during mixed infection hybrid genomes can result. They are joined near their 5’ ends, and perhaps in other regions as well, by hydrogen bonds.
All Retroviruses encode the four genes called gag, pro, pol, and env, which are always found in his order in the genome. The name gag comes from group-specific antigen, because the proteins encoded in this gene are more highly conserved, and therefore more widely cross reactive immunologically, than are the envelope proteins of the virion. The peptides derived from the Gag polyprotein, the precursor polyprotein encoded in the gag gene, form the capsid of the retrovirion. The pro gene encodes a protease (PR) that is required for the processing of Gag, and pol encodes three activities, RT,RNase H, and integrase (IN). RNase H forms a separate domain in the RT-RNase H protein, but functions as an integral component of RT. IN is required for the integration of the dsDNA copy of the retroviral genome into the host chromosome. The fourth gene, env, encodes the envelope glycoprotein at the surface of the envelope retrovirion. The primary product is Env, which is processed by cleavage to form an N-terminal external protein called SU (for surface) and a C-terminal protein that spans the membrane called TM (for transmembrane). The order of genes in the provirus is the same as in the viral genome.
As described above, the genomes of complex Retroviruses contain a number of regulatory genes in addition to these four basic genes present in all Retroviruses genes will be described later on the next post.
Labels: Natasya
FAMILY RETROVIRIDAE
The retroviruses are a very large group of viruses that infect invertebrates as well as vertebrates. Most of what we know about this group of viruses comes from studies of viruses that higher vertebrates. Hundreds have been studied and, although considerable divergences exist, they form a well-defined taxon. All are sufficiently similar to be classified as belonging to a single family, the Retroviridae. The family gets it name from the concept that these viruses use retrograde flow of information, from RNA to DNA, whereas the conventional flow of information in living organisms is from DNA to RNA.
The RTs of Retroviruses are the most highly conserved elements of these viruses and have been used to study the relationships among them. Lineage of fish viruses, now classified as members of the genus Epsilonretrovirus. Based on these sequence relationships, the Retroviruses that infect birds and mammals are classified into six genera. Of these, members of three genera are characterized as simple retroviruses, which encode only the genes gag, pro, pol, and env (and sometimes dut). The other three genera retroviruses of higher vertebrates, as well as the fish viruses, encode, in addition, regulatory genes that control their life cycle, and they are called complex Retroviruses. Notice that these regulatory genes independently entered the four different lineages of complex Retroviruses represented by the four different genera. Thus, recombination to acquire new functions has been an ongoing process in the Retroviruses. Also notice that the complex Retroviruses do not group together.
The Epsilonretroviruses are more closely related to the Gammaretroviruses, which are simple viruses, than they are to other complex Retroviruses, and the Deltaretroviruses, Lentiviruses, and Spumaviruses are not particularly closely related.
Members of the different genera differ in their structure as visualized in the electron microscope. The simple viruses were formerly classified on the basis of morphology into groups A, B, C, and D. The nucleocapsids of C-type viruses, now classified as Alpharetrovirus and Gammaretroviruses, assemble during budding, and the nucleocapsid is centrally located in the mature virion. The nucleocapsids of B-type and D-type viruses, now classified as Betaretroviruses, assemble before budding and the nucleocapsid is eccentrically located (type B) or bar shaped (type D) in the mature virion.
Eukaryotic genomes contain a very large number of genetic elements that are related to retroviral genomes. Retrotransposons encode RT and can move around within the genome by a process that uses reverse transcription and insertion, similar to what happens with Retroviruses. They are related to retroviruses but have no independent lives as viruses. Other elements in the eukaryotic genome contain additional Retrovirus-like genes and appear to have arisen by insertion of retroviral into the germ line at some time in the past. Some of these are still active, capable of giving rise to infectious Retroviruses, whereas others are defective. It is clear that this class of elements has been coevolving with the eukaryotes for a long period of time. The integrated copies of Retroviruses in the germline constitute a form of fossil record that allows us to trace the lineage of at least some retroviruses for 100 million years or longer. For other viruses, whether RNA or DNA, we can only trace ancestry for much shorter periods of time.
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INTRODUCTION
Two families of animal viruses utilize reverse transcriptase (RT) in the replication of their genome, the Retroviridae and the Hepadnaviridae.
The retroviruses have been intensively studied for years because researchers discovered early that avian Retroviruses have the ability to induce leukaemia and sarcomas in chickens. The study of these viruses led to the discovery of cellular oncogenes, of RT, and of mechanisms that regulate cycling of the animal cell, and several Nobel prizes have been awarded for work with the avian retroviruses.
Although clearly important for our understanding of biology, for many years after their discovery Retroviruses were in some ways biological curiosities because no human disease was known to be associated with Retroviral infection. This changed with the discovery of human T-cell leukemia viruses, now known as primate T-lymphotropic viruses (PTLV), which cause leukemia in man. More recently, the appearance of Human Immunodeficiency Virus (HIV) and of acquired Immunodeficiency Syndrome (AIDS) in the human population has dramatically altered our understanding of the disease-causing potential of retroviruses.
Labels: Natasya
Poxviridae ( History of smallpox and its eradication)
Tuesday, January 27, 2009/ 2:02 AM
Unique featues
Poxviridae is the largest family of viruses, which can be seen under a light microscope. It has linear dsDNA covalently cross linked at ends. Important characteristic of poxvirus is that it is remains stable for hours in air.
Poxvirus can be split into 2 major groups and they are
Bioterrorism
(watch the video on the how pox virus is used as bioterrorism)
Poxviridae is the largest family of viruses, which can be seen under a light microscope. It has linear dsDNA covalently cross linked at ends. Important characteristic of poxvirus is that it is remains stable for hours in air.
Poxvirus can be split into 2 major groups and they are
- Chordopoxviriniae(poxvirus of vertebrates) and
- Entomopoxvirinae( poxvirus of insects)
Clinical features
- human is the only host
- causes respiratory secretions
- causes skin lesions
- 12-7 days of incubation
- there are nine types of poxvirus that causes the disease
- variola (infects human) and vacinnia (infects cow)
- show inflenza like sympotoms
- form pustules which scars the skin
- if not treated it causes blindness or even
(watch the video on the features of small pox)
Vaccination
- Edward jenner was the first person came out the first vaccination for small pox
- used cow pox(vaccinia which is used as vector) from milkmaids
- to vaccinate james phipps
- and cured him
Eradication
- no reservoir for vaccinia or variola except man
- causes acute infection where the patients dies or obtains life long immunity
- is also an efficient immunogen.
Lab diagnosis, epidemology, control
- it was eradicated in 1980
- it was found to be infectious during symptoms and not during incubation.
- best defence against small pox was vaccination
- last outbreak in happened in yugoslavia in 1972
- after the outbreak the infectious materials was incinerated
- now the vaccination have stopped
Bioterrorism
(watch the video on the how pox virus is used as bioterrorism)
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Hepadnaviridae
Sunday, December 21, 2008/ 6:02 AM
Hepadnaviridae is a partial dsDNA virus that causes liver infections in humans and animals.
Source of picture: wikipedia.org
1) acute: subclinical-icteric-fulminant
- loss appetite, nausea, vomiting, jaundice, fever & abdominal pain
- most acutely-infected adults can recover
- however, some acutely-infected adults become chronically infected.
2) chronic: asymptomatic-chronic persistent- chronic active
- show no symptoms and no abnormalities in lab testing.
- others have chronically apparent chronic hepatitis
- some go on to develop cirrhosis
- HCC
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Herpesviridae
Herpesviridae is a linear dsDNA virus that causes disease in animals, including humans.
The members of this family are known as the herpesviruses.
In our syllabus, we learnt about :
-alphaherpes: HS1 virus, HS2 virus & varicella zoster virus
-betaherpes: cytomegalovirus
-gammaherpes: Epstein Barr virus
Source of figure: wikipedia.org
1) Herpes Simplex Virus: cold sores ard mouth(1wk), affects eyes & gums, genital herpes, burning sensation.
- HSV1 (cold sores) - oral cavity
- HSV2 (genital herpes) - genital
2) Varicella Zoster Virus: fever, lesion all over body, scratched lesion leads to secondary infection, scarring, affects nervous system.
- Varicella (chicken pox) - respiratory tract, pharynx
- Herpes Zoster (shingles) - 2nd infection
3) Cytomegalovirus - saliva, urine, semen, cervial secretion, breast milk
4) EBV - nasopharynx, salivary gland
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Virus Classification/Taxonomy
Wednesday, December 17, 2008/ 5:27 AM
This first post will be a summary on Virus Classification/Taxonomy.
Since viruses are largely pseudo-living in nature, they do not neatly fit into the biological classification system for cellular organism.
Therefore, virus classification is based on its genome or physical properties. The physical properties includes the nucleic acid of the virus, symmetry of capsid, dimensions of virion and capsid and the presence/absence of envelope.
The two types of classification are:
Lwoff's Scheme for Classification - which makes use the physical properties of the virus.
Baltimore's System for Classification - which makes use of the virus genome and its assoc. to mRNA.
Baltimore System for Classification
Virus can be placed in one of the following groups:
Class I: dsDNA viruses
Class II: ssDNA viruses
Class III: dsRNA viruses
Class IV: (+) sense ssRNA viruses
Class V: (-) sense ssRNA viruses
Class VI: ssRNA-RT viruses
Class VII: dsDNA-RT viruses
Source of figure: wikipedia.org
ICTV Classification
This system of classification combines both Lwoff's and Baltimore's as follows:
Order
Family
Genus
Species
-isolates
-strains
-variants
-types, subtypes
-serotypes
-etc...
Since viruses are largely pseudo-living in nature, they do not neatly fit into the biological classification system for cellular organism.
Therefore, virus classification is based on its genome or physical properties. The physical properties includes the nucleic acid of the virus, symmetry of capsid, dimensions of virion and capsid and the presence/absence of envelope.
The two types of classification are:
Lwoff's Scheme for Classification - which makes use the physical properties of the virus.
Baltimore's System for Classification - which makes use of the virus genome and its assoc. to mRNA.
Baltimore System for Classification
Virus can be placed in one of the following groups:
Class I: dsDNA viruses
Class II: ssDNA viruses
Class III: dsRNA viruses
Class IV: (+) sense ssRNA viruses
Class V: (-) sense ssRNA viruses
Class VI: ssRNA-RT viruses
Class VII: dsDNA-RT viruses
Source of figure: wikipedia.orgICTV Classification
This system of classification combines both Lwoff's and Baltimore's as follows:
Order
Family
Genus
Species
-isolates
-strains
-variants
-types, subtypes
-serotypes
-etc...
Labels: hidayah