Final answer:
The HIV life cycle involves the virus attaching to a CD4 receptor, fusing with the T cell membrane, converting its RNA into DNA, and integrating this DNA into the host's genome. New viruses are produced from the host's cellular machinery and the lack of proofreading in reverse transcription can lead to drug resistance. Genetic mutations such as CCR5A32 can provide resistance to HIV.
Step-by-step explanation:
The life cycle of HIV, a retrovirus, begins with the virus attaching to a CD4 receptor on the surface of a T cell. After attachment, the virus fuses with the cell membrane and releases its RNA and reverse transcriptase into the host cell. The reverse transcriptase converts the single-stranded viral RNA into complementary DNA (cDNA), and this newly formed DNA is then integrated into the host's genome by an enzyme called integrase. This integration allows the virus to remain dormant or to begin producing new viruses if the T cell is activated. During virus replication, the host cell produces viral mRNA, which leads to the production of new viral proteins and RNA genomes. These components are assembled into new virions, which bud from the cell, completing the cycle.
Certain genetic mutations, like the CCR5A32 mutation, can impede the HIV life cycle by preventing the virus from attaching to the CD4 receptors, thus providing some individuals with resistance to certain strains of HIV. On the other hand, the reverse transcriptase's lack of proofreading activity leads to mutations and can result in rapid development of drug resistance.
Managing HIV is particularly challenging as the virus not only targets essential immune cells but also incorporates itself into the host's DNA, making it difficult to detect and treat. Combination antiretroviral therapy (ART) is often employed to slow down the progression of HIV infection and reduce the chance of developing drug resistance.