HIV‐1 and hijacking of the host immune system: the current scenario

Abstract

Human immunodeficiency virus (HIV) infection is a major health burden across the world which leads to the development of acquired immune deficiency syndrome (AIDS). This review article discusses the prevalence of HIV, its major routes of transmission, natural immunity, and evasion from the host immune system. HIV is mostly prevalent in Sub-Saharan Africa and low income countries. It is mostly transmitted by sharing syringe needles, blood transfusion, and sexual routes. The host immune system is categorized into three main types; the innate, the adaptive, and the intrinsic immune system. Regarding the innate immune system against HIV, the key players are mucosal membrane, dendritic cells (DCs), complement system, interferon, and host Micro RNAs. The major components of the adaptive immune system exploited by HIV are T cells mainly CD4+ T cells and B cells. The intrinsic immune system confronted by HIV involves (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G) APOBEC3G, tripartite motif 5-α (TRIM5a), terherin, and (SAM-domain HD-domain containing protein) SAMHD1. HIV-1 efficiently interacts with the host immune system, exploits the host machinery, successfully replicates and transmits from one cell to another. Further research is required to explore evasion strategies of HIV to develop novel therapeutic approaches against HIV.

TRIM21 Restricts Coxsackievirus B3 Replication, Cardiac and Pancreatic Injury via Interacting With MAVS and Positively Regulating IRF3-Mediated Type-I Interferon Production

“…Recently, a growing body of evidence suggests that many TRIM proteins play important roles in direct antiviral activities and in the regulation of antiviral innate immunity. TRIM5α was found to inhibit HIV-1 replication by directly interacting with viral proteins ( 13 ). TRIM22 has been reported to exert antiviral activity against several viruses, such as hepatitis B virus (HBV), encephalomyocarditis virus (ECMV), and human immunodeficiency virus (HIV-1) ( 14 – 16 ).…”

The Future of Influenza Vaccines: A Historical and Clinical Perspective

“…Some pathogens that cause chronic infections, like Treponema pallidum (the causative agent of syphilis) and hepatitis B virus (HBV), are adapted for stealth, highly evolved to fly under the human immune radar for years. Others, like human immunodeficiency virus (HIV) and hepatitis C virus (HCV), take a less silent approach, instead actively interfering with immune response mechanisms on many levels [ 32 , 33 , 34 , 35 ]. For these diseases, vaccines are being called upon to stimulate an immune response against pathogens that are exquisitely well adapted to avoid immune-mediated destruction.…”

SERINC as a Restriction Factor to Inhibit Viral Infectivity and the Interaction with HIV

“…In this sense, the human immunodeficiency virus (HIV) is not the exception among retroviruses. The HIV has developed mechanisms to overcome these types of cellular barriers that hinder replication (the restriction factors) through viral proteins that interfere with, or nullify, the activity of the host's defense factors [ 12 , 13 ]. HIV uses its accessory proteins such as the Vif that counteracts the apolipoprotein B mRNA-editing enzyme 3G (APOBEC3G), Vpr for SLX4 endonuclease complex, Vpu for bone marrow stromal antigen 2 (BST-2) or tetherin, and Vpx for SAM-domain HD-domain containing protein 1 (SAMHD1) [ 14 – 19 ].…”