Conclusion

Studies have proven that vif, vpu, nef, and vpr genes of HIV-1 are not accessory genes as originally believed, but rather essential components in efficient and normal HIV-1 pathogenesis. Although the virus can replicate in the absence of these genes, their presence greatly improves the quality of infection. Vif is involved in the transport of virions into the nucleus and in stabilizing viral DNA intermediates. The Vpu protein is involved in the degradation of CD4 molecules in the ER and in the enhancement of virions released from the cells. Nef downregulates CD4 molecules on the cell surface and enhances viral replication. Vpr transports the viral preintegra-tion complex into the nucleus and freezes cell growth at the G2/M phase. Many of the functions of the accessory proteins overlap with one another, but the reason for this is still not clear.

The immunogenicity and low functional mutagenicity combine to make the accessory gene products attractive elements in the design of future antiviral immune therapeutics. A vaccine developed specifically against the accessory gene products will have to use an attenuated or mutated form of the protein since the wild-type proteins interfere with normal cell mechanisms. Studies on the interaction between the accessory proteins with various cellular factors are revealing new targets for antiviral therapies. The use of X-ray crystallography and rational drug design techniques will greatly improve the process of finding an antiviral therapy directed against the accessory gene products of HIV. Successfully mitigating the actions of the accessory genes of HIV could prove to be the key to stop this deadly virus.

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