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HIV can infect a variety of immune cells such as CD4 + T cells, macrophages, and microglial cells. HIV-1 entry to macrophages and CD4 + T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells' membrane and also with chemokine co-receptors. [25] [43]
The genome and proteins of HIV (human immunodeficiency virus) have been the subject of extensive research since the discovery of the virus in 1983. [1] [2] "In the search for the causative agent, it was initially believed that the virus was a form of the Human T-cell leukemia virus (HTLV), which was known at the time to affect the human immune system and cause certain leukemias.
HIV-1 is the more commonly associated with AIDS in the US and worldwide, HIV-2 is more rare, and typically restricted to areas in western Africa and southern Asia. HIV-2 is so uncommon that “HIV” almost always refers to HIV-1. Alright HIV targets CD4+ cells, meaning cells that have this specific molecule called CD4 on their membrane.
The human immunodeficiency virus (HIV) [8] [9] [10] is a retrovirus [11] that attacks the immune system.It is a preventable disease. [5] There is no vaccine or cure for HIV. It can be managed with treatment and become a manageable chronic health condition. [5]
Viral envelope persistence, whether it be enveloped or naked, are a factor in determining longevity of a virus on inanimate surfaces. [15] Enveloped viruses possess great adaptability and can change in a short time in order to evade the immune system. Enveloped viruses can cause persistent infections. [citation needed]
HIV can survive at room temperature outside the body for hours if dry (provided that initial concentrations are high), [31] and for weeks if wet (in used syringes/needles). [32] However, the amounts typically present in bodily fluids do not survive nearly as long outside the body—generally no more than a few minutes if dry. [23]
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HIV-1 fusion process. It involves both subunits of the envelope spike complex. Notably, gp41 is shown in green with its transmembrane region buried in the virion membrane, both segments of heptad repeats (CHR closer to the virus and NHR closer to the host cell) before and after conformational changes, and the N-terminal end of the ectodomain in ...