A cellular protease cleaves gp160 to generate gp41 and gp120, But I also keep on seeing the gp140,.adn also gp150,. is there any structural difference between them and gp120?
Hi, gp140 and gp150 ...etc these are variants or derivatives of gp160, usually created in the lab for vaccine/research purposes. The difference is that they can lack some componenets of the Env proteins, for example i believe gp140 lacks the transmembrane domain (TM) which is the gp 41. Hope that helps
HIV-1 envelope glycoprotein is synthesized as a precursor glycoprotein, gp160, and is then processed into gp120 and gp41. As Mohamed has mentioned, these are lab designed variants used for a successful vaccine development and for various neutralizing assays. gp140 is created by deleting trans-membrane and cytoplasmic domain namely gp140L, which contained the complete membrane-proximal external region (MPER), and gp140S, which lacks the distal half of MPER. Moreover, it has also been observed the neutralization sensitivity of gp120, gp140, and gp41 are distinct. Hope it clarifies your doubt.
The "core" of the HIV particle is encased in an "envelop" made of a bi-lipid membrane which bears the gp120 & gp41 antigenic epitopes sticking out as "trans-membrane glyco-proteins" (gp stands for glycoprotein). These structures (gp120 & gp41) bind to corresponding receptors (co-receptors) on the membrane T lymphocytes, monocytes, macrophages and CNS microglial cells to initiate the process of cell entry through fusion of host and viral cell membrane.
The binding to CD4 co-receptors by gp120 brings about an initial conformational change in the host cell membrane structure, but ultimate membrane fusion and entry into the host cell requires further interaction between CXCR4 & CCR5 chemokine co-receptors present on the host cell membrane and gp41 to allow the fusion of the two membranes.
Co-receptor genetic variation amongst individuals determine viral affinity for host cells: T-tropic HIV strains are attracted to T cells via CXCR4 co-receptor, M-tropic strains to macrophages via CCR5 co-receptor and Dual-tropic strains to both.
Mutations of CCR5 & CXCR5 have been shown to be protective against HIV entry into host cells.
Also Cytomegalovirus has been shown to predispose to "HIV resistance" probably attributed to the possession of receptors similar to human chemokine receptors (provides sanctuary for HIV).