With a frightening and a practically 100 percent efficiency the HIV retrovirus uses only a negligible part of its genetic code to get protection from carrier organism cells and to infect new healthy cells.

These are results of a research conducted by scientists of Dana Farber Cancer Institute. They have discovered a way in which retrovirus leave an infected cell and hides in its membrane in order not to be killed by organism’s immune system.

Virus is one of the most mysterious and misunderstood organisms. Virus is able to produce performance of beings only in cells. In fact, virus is an intracellular parasite which is not able to breed outside a cell. While all cellular organisms mandatory have two nucleic acids, namely, the DNA and RNA, a virus has only one of the two. Regardless of the nucleic acid virus contains, the acid carriers genetic information. Based on this fact, all viruses are classified in two large groups, namely, DNA-containing and RNA-containing viruses.

Unlike cellular organisms, viruses don’t have their own metabolic system, including a system for protein synthesis. Viruses introduce in a cell only their own genetic information. A DNA and RNA virus matrix helps to synthesize informational RNA which is a base for transforming virus proteins by ribosomes of an infected cell. Virus’ DNA molecule, or virus genom, is able to build in a master’s cell genom and to exist in this form; it may play a role of additional gene or even be hidden over there for indefinite time.

For the time being, scientists have been studying mechanisms which newly-originated viruses use to leave “mother cells” wherein they were born (scientists call it “the late domain”). This domain “turns on” at the final stage of the process, when newly-born viruses are “packing suitcases”, i.e. when they are gathering on the cell membranes immediately before leaving it to infect other cells to reproduce again.

The mechanism functions as follows. Viruses, circulating in organism’s liquid, penetrate by chance inside a cell together with intracellular liquid drops. However, as a rule, before viruses begin penetrating inside, they are bonded with a special protein receptor on the cell wall. Special proteins on the virus cell wall which “identify” a respective receptor on the surface of a sensitive cell help to effect adhesion process. A part of the cell wall virus has been attached to is placed in a cytoplasm and is transformed into a vacuole. The originated vacuole with a cytoplasm membrane wall, can merger with other vacuoles or a nucleus. That’s the way virus is transported to any part of a cell.

Infection process starts with a penetration of a virus in a cell, wherein it then breeds. Virus genom is reduplicated and a capside is automatically mantled. To reduplicate, nucleic acid has to get rid of a shell. In addition to reduplication, genom virus participates in a synthesis of the RNA required for forming capside proteins on a mother cell robosomes. When a new nucleic molecule have been synthesized, it is covered with proteins. Having accumulated, virus particles then exile from the cell. For some viruses, this process is effected in the form of a “blast” which breaks integrity of the cell; as a result, the cell dies. Other viruses are reproduced in a way, similar to budding; in this case, organism’s cells can save their vital activity for a long time.

In the case described herein, a virus which first infects a cell, builds-in into its reproductive mechanism and produces thousands of its copies and then accumulates the born clones was investigated. Not completely mature and active viruses comprise only RNA molecules which are gathered inside the cell membrane; it’s like waters charge at a damp. As a result, the cell membrane starts bloating and its shell, blocking RNA virus from entering another part of the cell, bursts out in the end. (Ref. to Fig.). Thousands of newborn viruses immediately adhere to the membrane outer wall, waiting for the time when they can slip down and catch neighboring healthy cells.

Ten years ago, scientists found that the clones of the pressure HIV retroviruses put on a cell membrane was insufficient for viruses to get out of the membrane boundaries. This new research fills in a gap in understanding the domain mechanism operation which viruses use to leave mother cell at the last stages of their development. At the last stage, handfuls of molecules are accumulated, with amino acids of pyrrolydine-alpha-carbon acid (PACA) in the first place.

Fig. Virus development mechanism

The final results of the research have shown that majority viruses, including HIV, use the same or similar mechanism to separate from a cell membrane. Discovery of the PACA made it possible to concentrate strictly on this investigation area to study domain operation. Scientists suppose that molecules of these acids play a role of a target (a bait) for cell proteins which help viruses to separate from a cell membrane at the time when the cell is busy with a processing of bait molecules, and set free in the end.

This capability of a virus allows it to receive a huge advantage in comparison with a protective ability of a cell. The more scientists know about the mechanism, the sooner we’ll be able to produce a vaccine to stop virus development at the stage when a virus is leaving a cell. For such kind of a therapy, antibiotics which themselves are harmful to healthy cells won’t be required.

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