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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.
While the mechanisms are not clearly understood for HIV-1 and HIV-2, it is known that they use different pathways and patterns, making the algorithms used to evaluate HIV-1 resistance-associated mutations irrelevant to HIV-2. [34] Each virus can be contracted individually, or they can be contracted together in what is referred to as co-infection.
A negative result rules out HIV exposure, while a positive one must be followed by an HIV-1/2 antibody differentiation immunoassay to detect which antibodies are present. This gives rise to four possible scenarios: 1. HIV-1 (+) & HIV-2 (−): HIV-1 antibodies detected; 2. HIV-1 (−) & HIV-2 (+): HIV-2 antibodies detected; 3.
A small proportion of humans show partial or apparently complete innate resistance to HIV, the virus that causes AIDS. [1] The main mechanism is a mutation of the gene encoding CCR5, which acts as a co-receptor for HIV. It is estimated that the proportion of people with some form of resistance to HIV is under 10%. [2]
SARS-CoV-2 and HIV-1 have similarities—notably both are RNA viruses—but there are important differences. As a retrovirus, HIV-1 can insert a copy of its RNA genome into the host's DNA, making total eradication more difficult. [156] The virus is also highly mutable making it a challenge for the adaptive immune system to develop a response.
Resistance to a drug. A resistance mutation is a mutation in a virus gene that allows the virus to become resistant to treatment with a particular antiviral drug.The term was first used in the management of HIV, the first virus in which genome sequencing was routinely used to look for drug resistance.
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