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The journey of HIV disease

The development of AIDS depends on the ability of the HIV virus to destroy your immune system and the inability of the immune system to destroy HIV. HIV disease begins with an acute infection that can not be completely resolved by an adaptive immune response and continues to become a chronic and progressive lymphoid tissue infection. The course of HIV disease can be followed by examining the amount of virus in plasma and the number of CD4 + T cells in the blood. Primary HIV infection of the fetus and neonate occurs in immature immune system situations, so the following explanation is a typical pathogenesis illustration that can be followed in adults. Primary infection occurs when virions of HIV in the blood, semen, or other body fluids from a person enter into another’s cell through a fusion mediated by gp120 or gp41 receptor. Singapore HIV Clinic uses the latest and current ART drug regimen that has a better side effect profile. We avoid the cookie cutter mindset because we understand that each patient has a very different medical background and will react differently to different antiretroviral drugs.

Dendritic cells in the epithelium where virus entry will catch the virus then migrate to the lymph nodes. Dendritic cells express proteins that play a role in the binding of the HIV envelope so that dendritic cells play a major role in the spread of HIV to lymphoid tissue. In lymphoid tissue, dendritic cells can transmit HIV to CD4 + T cells by direct contact between cells. A few days after the first exposure to HIV, viral replication in large quantities can be detected in the lymph nodes. This replication causes viremia accompanied by acute HIV syndromes (nonspecific symptoms and signs such as other viral infections). Viruses spread throughout the body and infect subset cells of CD4 or T helper, macrophages, and dendritic cells in the peripheral lymphoid tissue. After the spread of HIV infection, there are both humoral and cellular adaptive immune responses to viral antigens. The immune response can control some of the infections and viral production, leading to reduced viremia within 12 weeks after the first exposure. After acute infection, there is a second phase in which the lymph nodes and spleen become the site of HIV replication and cell destruction. At this stage, the immune system is still competent in overcoming opportunistic microbial infections and has not yet emerged clinical manifestations of HIV infection, so this phase is also called clinical latency period. In this phase the amount of virus is low and most of the peripheral T cells do not contain HIV. Nevertheless, the destruction of CD4 + T cells in lymphoid tissue continues and the number of circulating CD4 + T cells decreases.