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AIDS/Acquired Immunodeficiencies – VI
This Sqadia video demonstrates about AIDS and other Immunodeficiencies. During this stage of the disease, HIV continues to multiply in the body but at very low levels. People with chronic HIV infection may not have any HIV-related symptoms, but they can still spread HIV to others. In Chronic phase of infection, Virus is kept in check. Level of virus in circulation after six months of infection is a good predictor of the course of disease. In many cases, the structure of the lymph node had been completely destroyed by virus. This destruction takes place long before plasma viral load increased above the steady-state level. Direct viral infection and destruction of CD4 T cells. Half-life of an actively infected CD4+ T cell is less than 1.5 days. There are smaller numbers of CD4+ T cells that become infected, but do not actively replicate virus. Proviral DNA replicates in cell division along with cell DNA. Studies in which viral load is decreased by antiretroviral therapy, concurrent increase in CD4 T cell numbers.
AIDS/Acquired Immunodeficiencies – VII
Not only depletion of CD4+ T cells but other immunologic consequences can be measured in HIV-infected individuals during the progression to AIDS. These include a decrease or absence of delayed hypersensitivity to antigens to which the individual normally reacts, increase in the serum levels of immunoglobulins, especially IgG and IgA. Generally, the HIV-infected individual loses the ability to mount T-cell responses in a predictable sequence: responses to specific antigens (for example, influenza virus) are first lost, then response to alloantigens declines, and lastly, the response to mitogens such as concanavalin A or phytohemagglutinin can no longer be detected. HIV-1 infected individuals often display dysfunction of the central and peripheral nervous systems. Specific viral DNA and RNA sequences have been detected by HIV-1 probes. Quantitative comparison of specimens from brain, lymph node, spleen, and lung of AIDS patients with progressive encephalopathy indicated that the brain was heavily infected. Development of a vaccine to prevent the spread of AIDS is the highest priority for immunologists. There are several strategies for development of effective anti-viral drugs. The key to success of such therapies is that they must be specific for HIV-1 and interfere minimally with normal cell processes. Two types of antiviral agents are Reverse Transcriptase Inhibitors and Protease Inhibitors.
AIDS/Acquired Immunodeficiencies - VIII
Several antiretroviral drugs either interfere with reverse transcription or inhibit the viral protease. The prototype of the drugs that interfere with reverse transcription is zidovudine, or AZT (azidothymidine). The introduction of AZT, a nucleoside analog, into the growing cDNA chain of the retrovirus causes termination of the chain. A second class of drugs called protease inhibitors has proven effective when used in conjunction with AZT and/or other nucleoside analogs. Current treatment for AIDS is a combination therapy i.e HAART. HAART stands for highly active anti-retroviral therapy. Two nucleoside analogs and one protease inhibitor is used in most cases. In many cases, HAART has lowered viral load to levels that are not detectable by PCR. Most AIDS experts are not convinced that this is possible to eradicate all virus and thus actually cure AIDS, mainly because of the persistence of latently infected CD4+ T cells and macrophages, which can serve as a reservoir of infectious virus if the provirus should be activate.
AIDS/Acquired Immunodeficiencies - IX
The present expense of HAART, strict regimen and side effects precludes universal application. Even if eradication of the virus in individuals treated with combination therapy becomes possible, it will not greatly influence the epidemic in the developing countries. At present the best option to stop the spread of AIDS is a safe, effective vaccine. The infection by HIV-1 and progression to immunodeficiency syndrome flourishes even in the presence of circulating antibodies. Immunity may hold the virus in check for a time, it rarely exceeds 12 years. Most vaccines prevent disease, not infection. Polio and influenza vaccines hold the virus produced by infected cells in check so that it does not cause harm to the host, and it is then cleared. HIV-1 does not fit this model, because it integrates into the host genome and may remain latent for long periods. Most vaccines prevent infection by viruses that show little variation. The instability of its genome differentiates HIV-1 from most viruses for which successful vaccines have been developed, with the exception of influenza.
AIDS/Acquired Immunodeficiencies – X
The majority of successful vaccines are live-attenuated or heat-killed organisms. The development of a live-attenuated retrovirus vaccine from animal viruses engineered to include HIV antigens is a possible route. However, the use of live vaccines is predicated on the supposition that the immunity raised will clear the vaccine virus from the host. This is not easily done for a retrovirus, which integrates into the host genome. For most viruses, the frequency of exposure to infection is rare or seasonal. In many high-risk individuals, such as commercial sex workers, monogamous sexual partners of HIV infected subjects, and intravenous drug users, the virus is encountered frequently and, potentially, in large doses. The most common route of HIV-1 infection is by the genital tract. Testing a vaccine for safety and efficacy normally involves challenge of an animal with the virus under conditions similar to those encountered in the human. In this way, the correlates of protective immunity are established.