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Transmission of HIV infection6. Transmission of HIV infectionThe HIV infection can be transmitted by the percutaneous route, by sexual contact either homoxesual or heterosexual, from infected mother to her child. At present there is no evidence that the virus can be transmitted through casual contact with an infected individual such as family contacts, food or water, blood-sucking insects, airborne or faeco-oral routes.Transmission by blood transfusion The first case of transfusion associated AIDS was described in an infant given transfusion for erythroblastosis foetalis. It is now established that HIV infection can be transmitted by infected blood and blood components, including plasma and factor concentrates. The risk is markedly increased particularly in products prepared from donor pools. Post transfusion AIDS has been reported especially in haemophilics but other multi-tansfused patients are also known tobe affected.’ Incidence of transfusion associated AIDS is about 2-3% of all AIDS cases. However in cases of transfusion related AIDS. history of blood transfusion in preceding 5 year period is relevant. Patient with multiple transfusions, massive transfusion and those receiving pooled plasma products are at markedly increased risk of acquiring HIV infection through transfusion. Before the introduction of screening of donor plasma for HIV-antibodies and heat treatment of certain plasma products, coagulation factor VIII concentrates had effectively spread the infection to patients with haemophilia. Infection of the recipient is apparently invariable following transfusion of a blood unit contaminated with HIV and the efficiency of transmission of HF) is 90% from a single blood unit. Prevention of transmission of H1V through blood transfusion HIV screening After the relation between blood transfusion and HIV infection was established, many countries passed a legislation that only blood and blood products found non-reactive for HIV-antibodies should be àsed for transfusion. Unlike other infections, the antibodies which appear following HIV infection have no protective role and are unable to neutralize the virus. Although the antibodies are not protective, they serve as a very useful marker of infection. The presence of the antibody indicates presence of virus and thus implies infectivity. In spite of the screening tests for anti-HIV an individual who may have just acquired the infection, may not seroconvert for periods upto 6-8 months or more. However HF)- antibodies are demonstrable in most infected people by 6-12 weeks after infection, bloood donation collected during this period between HIV infection and appearance of circulating antibodies (window period), may be infectious despite a negative antibody screening test. To achieve the objective of blood safety it is therefore very important to combine screening with other efforts to exclude donations from individuals with associated high risk factors. (Also refer to Section 9 Transfusion safety and optimal utilization of blood) In transfusion practice, the screening tests are used to detect asymptomatic healthy carriers. All the screening tests are based on the demonstration of specific antigen-antibody complex. The tests normally used are enzyme immunoassays using viral antigens from viral lysates, recombinant or synthetic antigens and a mixture of antigen for HIV-1 and/or HIV-2, based on competitive/sandwich ELISA system. Acquired Immunodeficiency Syndrome (AIDS) Acquired immunodeficiency syndrom (AIDS) is a disease complex in which the affected perosn’s defence merchanism is compromised, making the individual extremely susceptible to opportunistic infections and/or malignancies. Although the disease and its causative agent has been known to the world only since 1980 its serious implications on the social and economic structure globally have made it a target of extensive reasearch. Clinical disease and its consative agent HIV was first isolated from the cells of an infected patient in 1981 and was subsequently identified as the causative agent of AIDS. It was named as HTLV-III (Human T-cell lymphoma virus-III), LAY (lymphadenopathy associated virus) and finally renamed in 1983 as Human immunodeficiency virus (HIV). HIV is a slow retrovirus (lentivirus), The characteristic of a etrovirus is that it posesses RNA as the genetic material 4not DNA) and carry an enzyme Reserve Transcrie which catalyses transcription of RNA into DNA. The HIV génome consists typically of three retroviral genes, which are as follows.
Recently a second, similar but distinct virus, HIY-2 has also been shown to be a causative organism for AIDS. HIV-2 was identified in 1985 in West African high risk population and has the same mode of transmission as HIY-1. HIV-2 differs from HIY-1 in the molecular weight of different Proteins These differences from the basis of distinguishing HIY-1 from HIY-2. However, since most I-flY-i kits cssreact with HIY-2 antibodies, more sophisticated techniques e.g., synthetic peptide immunoassay & pdlyerase chain reaction (PCR) are necessary to identify HIY-2. At present, sporadic reports of HIY-2 infection have been documented from Maharastra & Tamilnadu and it is likely to be a major public health problem in the near future. The HIV shows selective tropism for CD-4 positive T lymphocytes with which it binds. Once bound, the virus uncoats and is able to transcribe its genomic RNA to DNA by the help of the enzyme reverse transcriptase. The proviral HIY DNA is then integrated in the genome of the T4+ lymphocyte. The viral genome may remain integrated in the host cell DNA for a long time without producing any effect. The retrovirus integrates into the infected cell as pro-virus and each time the cell creplicates, it carriers the viral enome with it. Therefore, the individuals who are infected with retroviruses are permanently affected. The incubation peroid may be a few month to more than 5-7 years. Many HIV+ve persons remain asymptomatic for a variable period of time, but are capable of transmitting the infection to others. Clinical manifestation. The following clinicaistages are seen in HIV infection 1. Storage of acute seroconversion illness 2. Asymptomatic carrier stage 3. Persistent generalized lymphadenopathy (PGL) 4. HIV constitutional disease & AIDS related complex (ARC) 5. Full blown AIDS Serological & biochemical findings in AIDS Seroconversion in sequential samples of an individual most positively points to the Individual having recently been infected. Following infection antibodies may appear anytime within 6 weeks to 6 months.: The most immunogenic proteins against which antibodies can be detected are p24 (core) and gp 41(invelope). Window Period It should be appreciated that following infection and prior to development of antibody there is a ‘window period’ of varying length, during which the infection establishes. At this point of time the antibody has yet not developed. The window period is short and within about 6-12 weeks antibodies (IgM) appear. The emergence of antibodies corresponds with a decrease in free Ag. The levels of antibody to p24 & gp4l (IgG) peaks and remain constant throughout the stages of asymptomatic infection and persistent generalized lymphadenopathy. Epidemloiogy of HIV infection The following group of individuals are at a much higher risk of acquiring and transmitting HIV infection i.e. a. Heterosexually / homosexually promiscuous b. Intravenous drug addicts c. Recipients of pooled blood products d. Sexual contacts of the above categories.
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