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