Life Cycle, Replication and Regulation of Gene Expression

Sakti Prakash Patra^*
*Correspondence: Sakti Prakash Patra, Delta College, India, Email:

Keywords

Life Cycle, Gene Expression, DNA, RNA, HIV.

The goal of this chapter is to provide a brief summary on the "life" cycle of HIV, which should maybe be better referred to as the viral "answer/copy" cycle, since viruses do not have their own chemically processing and using food and are this way usually not thought about/believed living things. Viruses can be thought about/believed as within cell things that feed off of, and weaken, other things that are strictly dependent on living host cells for reproduction. Understanding how HIV interacts with its target cells in order to copy is of great interest because it may provide important clues for the generation of improved HIV/AIDS-fighting drugs and the development of new success plans/ ways of reaching goals to control or even eliminate the virus. The main targets of HIV are CD4+ helper T cells, which are key devices that control things/ groups of people that ensure rules are followed of the humoral and cellular unable to be harmed responses. So, their destruction and using everything up completely by machines/methods/ways that are not fully understood make the body unable to defend itself against grabs at any easy opportunity things that cause disease. When HIV infects an activated CD4+ T cell, it hijacks and controls/moves around/misleads its written version of spoken words al and translational machinery to reproduce itself. As briefly organized and listed below and specified in the following chapters, HIV has to use a large number of cellular factors and to oppose/to go againstact the HIV/AIDS-fighting activity of others in order to complete its answer/copy cycle.

Probably but not definitely, each interaction with cellular factors that are extremely important for virus answer/copy termed "virus-dependency" factors or strengthening of HIV/AIDS-fighting or "host restriction" factors. As described below, CD4 is the first or most important receptor, and the chemokine receptors CCR5 and CXCR4 are the main co-receptors of HIV entry Fusion. These receptors are good enough to make/give cells easily able to be harmed or influenced by HIV entry and so decide/figure out the viral cell tropism. However, the densities of the Env trimers on the virions and of the CD4 receptor on the target cells are often low. So, viral attachment is often inefficient and a limiting step for HIV infection. What's more, they may trap viral particles at the cell surface to make steady/make firm and strong them and to help settle an argument Tran's infection of able to be harmed or influenced T cells. For example, some say that dendritic cells DCs bind HIV virions at the site of related to sex organs exposure and transport them to the small areas in the body that fight disease where they help settle an argument both trans infection and stimulation of T cells that results in huge virus production.