How HIV infects the body and the lifecycle of HIV | AVERT
index-art.info fills you in on the topic, how does the hiv virus affect the helper t cell, with a wealth of fact sheets, expert advice, community perspective, the latest . CD4 cells are sometimes also called T-cells, T-lymphocytes, or helper cells. The CD4 cell count of a person who does not have HIV can be anything between But these factors don't seem to make any difference to how well your immune. CD4 T-cells are considered "helper" cells because they do not neutralize infections but rather triggers the body's response to infections like HIV.
Even when responses to autologous virus are measured, the initial detectable response has usually been to only one to three epitopes Goonetilleke et al. An important caveat is that there may be much more happening in the tissues than is sampled in the blood in these early stages. Even so, there is a clear hierarchy in initial responses and immunodominance that correlates with set point viremia, which is lost during the transition to chronic infection Streeck et al.
Although functional studies of early CTL responses are few Ferrari et al. By single genome amplification one can detect viral evolution at sites of CTL pressure as early as peak viremia Goonetilleke et al. These clearly occur in the setting of acute phase proteins and proinflammatory cytokines Stacey et al.
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- How Does The Hiv Virus Affect The Helper T Cell
- The T-Cell Response to HIV
The initial response is narrowly directed, predominantly at epitopes in Env and Nef, regions that are among the most variable in the virus Lichterfeld et al. Indeed, early responses appear to be targeted to epitopes of higher entropy for reasons that are not clear Bansal et al.
The breadth of responses increases over time, as do the number of HLA alleles that are involved in recognition of infected cells Altfeld et al.
Some acute phase epitopes are not those that are targeted in chronic infection and may be novel Goonetilleke et al. Often these earliest responses fade away as soon as the epitope escape has occurred. Although these detailed findings have been made in just four patients, ongoing studies in a further 12 show very similar patterns N Goonetilleke, M Liu, and AJ McMichael, unpubl. The influence of host genetics on acute phase CTL responses is readily apparent.
HLA alleles associated with protection from disease progression are preferentially targeted in acute infection, whereas coexpression of risk alleles does not induce responses, a process called immunodominantion Altfeld et al.
Association between HIV-specific T helper responses and CTL activities in pediatric AIDS.
Clinical symptoms of acute infection have been shown to be reduced in persons expressing HLA B57, and this allele is associated with improved outcome and also dominates the early response in persons who express it Altfeld et al. At least one study indicates the selective loss of high-avidity CTLs in acute infection, and when these are maintained they are associated with a lower viral load Lichterfeld et al.
There has been considerable interest and some controversy over whether highly exposed but HIV seronegative people, such as sex workers in high-HIVprevalence communities, make CTL responses to HIV-1 and whether these are helping them avoid infection Rowland-Jones et al. More likely, as shown by Ritchie et al.
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However, there is no evidence that either of these T-cell responses is protective. The relationship between the earliest CTL responses, viral set point, and disease progression remains controversial.
Kinetics of immune responses in acute infection are associated with serial waves of responses Turnbull et al. This may be caused by localization of responses at inductive and effector sites within lymphoid and gut mucosa, respectively, and responses detected in lymph nodes precede those detectable in peripheral blood and are of higher magnitude Altfeld et al.
There is a high predictability of initial and subsequent epitopes targeted, based on the HLA type of the individual Goulder et al. Remarkably, most responses detectable at the time a quasi-set point is achieved persist even in very late stage infection Koibuchi et al.
Specificity of responses during the chronic phase of infection repeatedly suggests that Gag targeting is associated with lower viral load Edwards et al. Helper T cells can stimulate another group of white blood cells called B cells to produce antibodies that bind that specific antigen and immobilize it, preventing it from causing infection. Antibodies are specific for only one antigen.
B cells must interact with Helper T cells, other specialized white blood cells, to initiate antibody production.
An important concept is that once activated, memory cells are produced that insure that a more rapid and stronger immune response can be made upon re-exposure to the same pathogen.
This is why vaccinations provide lasting protection against disease. These cells migrate and reside in the mucus membranes of our body. Pathogens viruses or bacteria that escape antibody detection can enter and infect cells. The surface of infected cells changes, and this change is recognized by T cells. Cytotoxic T cells kill infected cells, preventing these cells from producing more pathogen.
The T-Cell Response to HIV
Cytotoxic T cells must interact with Helper T cells to regulate destruction of infected cells. Without an adequate supply of Helper T cells, the immune system cannot signal B cells to produce antibodies or Cytotoxic T cells to kill infected cells.
When HIV has critically depleted the Helper T cell population, the body can no longer launch a specific immune response and becomes susceptible to many opportunistic infections.
This immunodeficiency is described in the name acquired immunodeficiency syndrome, or AIDS. Thus, our memory cells are rapidly infected and destroyed in the mucus membranes of our tissues.