Question

What would be the immunodominant antigens in the structure of HIV?

How does the new strain of HIV from gorillas (“P” variant) replicate compared to other strains? What would this mean for how the virus acts within the host?

Answer 1

Immunodominant epitopes of HIV-1 p17 and p24 :-

Immunodominant antibody-binding sites were mapped using overlapping synthetic peptides of the structural proteins p17 and p24 of human immunodeficiency virus type 1 (HIV-1). Using sera from HIV-1-infected individuals at a variety of disease states, three major epitopes were identified within p17 and one within p24. Antibodies which recognized these epitopes were present in all risk groups throughout all stages of HIV infection, regardless of the presence of high levels of serum p24 antigen.

New HIV strain originated in gorillas:-

Chimps are not the only animals that can harbor and introduce HIV into human populations, according to a new report. A 62-year-old woman, who recently arrived in Paris after living in Cameroon, is thought to be the first human to carry a strain of HIV originating in a gorilla.

The woman most likely got the virus from another person, since she claims not to have made contact with gorillas or meat from wild animals. This suggests she is not an isolated case. In fact, the authors note in Nature Medicine that the virus “could be circulating unnoticed in Cameroon or elsewhere.”

The new HIV strain is called RBF 168—or more simply the “P” variant of HIV—and is likely linked to a virus recently discovered in wild gorillas, according to the Nature Medicine paper. It joins three previously identified variants of HIV that originated in chimpanzees: M, N and O. (The M variant accounts for the majority of infections worldwide.) The authors observed that P replicates more rapidly than any of the other strains, which could mean that the virus has adapted to human cells.

HIV virus acts with in the host:-

Like other living things, viruses need to be able to reproduce.

When viruses reproduce it is called replication. HIV uses CD4 immune cells to replicate. And each infected CD4 cell produces hundreds of new copies of new HIV particles.

The process is called the HIV lifecycle.

(1.)Each replication cycle only lasts 1 to 2 days. It has several stages and different HIV drugs are active at different stages. HIV drugs are called inhibitors because they inhibit or stop parts of the cycle.

(2.)HIV first has to attach to a CD4 cell. The proteins on the outer surface of HIV (called gp41 and gp120) connect with receptors on the surface of the CD4 cell (usually the CD4 receptor and the CCR5 oreceptor).

(3.)HIV drugs that block this process are called entry inhibitors. This family of drugs block attachment to gp41 or gp120 on the CD4 receptor or block the coreceptor CCR5. Monoclonal antibodies (mAbs) can also block this stage.

(4.)After HIV attaches to the CD4 cell, it is absorbed into the main body of the cell. As this happens, HIV first loses its outer shell. This leaves viral capsid with HIV and three key enzymes (a type of protein) that HIV uses to replicate. Most scientists say capsid releases its contents into the cell for the RT stage (see below). But new group thinks HIV DNA is made inside the capsid, and that is is then released directly into the cell nucleus.

(5.) The first enzyme is called RT. This stands for reverse transcriptase. RT changes the single strand of HIV (called RNA) into a double strand to fit in with human DNA. Two different types of RT inhibitors (RTIs) block this process: (i) nucleoside/tide (NRTIs/NtRTIs), and (ii) non-nucleoside (NNRTIs).

(6.)The new double-stranded HIV crosses into the central nucleus of the CD4 cell. This is where HIV is integrated into human DNA. Drugs that block this process are called integrase inhibitors, abbreviated to INIs or INSTIs.

(7.)The CD4 nucleus then starts producing raw material to make new HIV. These long strands of new HIV particles need to be cut up and assembled as new virus. The enzyme involved in the cutting and assembling process is called protease. The HIV meds that block this process are called protease inhibitors.

(8.)The newly formed virus then has to leave the cell. Although there are currently no HIV drugs that block this stage, several drugs are in development. Budding inhibitors stop new HIV from leaving of the CD4 cell. Maturation inhibitors block the final assembly process.

(9.)The newly released viruses (called virions) go on to infect new CD4 cells – to repeat the process over again. The old CD4 cell then dies. This continuous process happens millions of times every day when not on ART. Without ART, HIV is one of the most active and rapidly reproducing virus.

An important concept about ART, is that HIV drugs only work on CD4 cells in your body that are awake and actively producing HIV.

However, most CD4 cells in your immune system are sleeping or resting. The resting cells, even if they contain HIV, are not affected by ART.