Threats due to HIV


Journal of Antivirals & Antiretrovirals primary current therapeutic approach against viral diseases is to target viral components that are essential for replication. There are a number of disadvantages targeting viral components including the limited number of druggable viral targets because viruses have a small genome, as well as the rapid development of drug resistance. New drug therapies combine antivirals to increase efficacy and to avoid the development of drug resistant strains. These strategies are effective for viruses such as HIV, but clearly there is a need to expand our drug arsenal to address the wide diversity of viruses. This pathway relies on alternative strategies for drug discovery, such as examining the virus-host interface. 

HIV stands for human immunodeficiency virus. It harms your immune system by destroying the white blood cells that fight infection. This puts you at risk for serious infections and certain cancers. AIDS stands for acquired immunodeficiency syndrome. It is the final stage of infection with HIV.

Dr. Deepak Kaul from Experimental Medicine and Biotechnology Department, Postgraduate Institute of Medical Education and Research, Chandigarh, India has done research on how HIV-1 Exploits Cellular miR-2909 RNomics to Initiate and Ensure AIDS Disease He stated his opinion as Human immune cells have evolved with a membrane trDٹckLnJ pathway called Autophagy, responsible for enJulfinJ the invading pathogens and thereby equipping these cells with the innate and adaptive immune responses against numerous pathogens. On the other hand, the various pathogens have developed strategies to either block or use the autophagy mechanism to their own advantage [1]. Human LmmunodeficLenc\ virus type 1 (HIV-1) infects mainly CD4+ Tlymphocytes and macrophages through the interaction of the viral (Env) glycoproteins (Gp120 and Gp41) with CD4 as well as coreceptor, mainly CCR5, expressed at the surface of the target cells. Such type of interaction induces a structural rearrangement in glycoprotein 41 and the insertion of its N-terminus fusion peptide into the target cell membrane, leading to the cellular endocytosis of the HIV-1 viral particles [2]. Нe HIV-1 replication cycle is governed in two phases: the early phase, from viral entry to provirus integration with cellular genome, and the late phase, from transcription of viral genes to the release of new particles.

Robert Har
Associate Editor
Journal of Antivirals & Antiretrovirals