HIV-1 MN ENV Fragments

The molecular weight of Env protein is 160 KD, so it is also called gp160. The initially synthesized Env is aggregated in the endoplasmic reticulum, then transferred to Golgi for glycosylation, and then cut into two smaller proteins, gp41 and gp120, by proteases in the cells. Gp41 contains the transmembrane region of Env, which is deeply located in the lipid bilayer of the newly synthesized toxic particles, while gp120 is located on the surface of the toxic particles and infected cells, and connects with gp41 by the non-covalent bond. The whole Env protein exists in the form of trimer on the surface of toxic particles and infected cells. The infection of the HIV virus to target cells begins with the interaction between virus particles and cell surface mediated by gp120. Gp120 can interact with CD4 and DC-SIGN on the surface of target cells, and then gp41 mediates the binding of viral envelope to the cell membrane to transport viral inclusions into the cytoplasm of infected cells.

Mechanism of ENV

During infection, the Env gene can evolve to encode a protein that alters the use of receptors and co-receptors, allowing the virus to enter another host cell. The gene expression of REV is regulated by the gene product of rev. Experimental deletion of rev leads to the undetectable expression of ENV protein and the decrease of Env mRNA expression in the cytoplasm. However, when the total cellular RNA was analyzed, there was no significant difference in the presence and absence of rev co-expression. The results showed that Env RNA in the nucleus increased significantly in the absence of rev expression, indicating that rev plays an important role in the nuclear output of Env mRNA. The role of rev has been further elucidated. It has been found that rev can transact on a specific sequence in the Env gene of HIV-1, thus initiating the output of incomplete spliced HIV-1 RNA from the nucleus.

Conclusion

HIV-1 relies entirely on environmental proteins to enter the cell. The virus usually replicates in activated CD4⁺ T cells because of the high surface level of the virus entering CCR5 coreceptors and CD4 receptors. During infection, the Env gene can evolve to encode a protein that alters the use of receptors and coreceptors, allowing the virus to enter another host cell. The identification and identification of such HIV-1 variants may contribute to early detection in order to intervene to reduce viral pathogenesis in these alternative cell types.

References

1. Bera, T. K., Kennedy, P. E., Berger, E. A., Barbas, C. F., & Pastan, I. (1998). Specific killing of HIV-infected lymphocytes by a recombinant immunotoxin directed against the HIV-1 envelope glycoprotein. Molecular medicine, 4(6), 384-391.
2. Kafando, A., Fournier, E., Serhir, B., Martineau, C., Doualla-Bell, F., Sangaré, M. N., ... & Tremblay, C. L. (2017). HIV-1 envelope sequence-based diversity measures for identifying recent infections. PloS one, 12(12), e0189999.