Abstract
Immunosuppression due to HIV infection is a resultant of several factors including defective innate signaling pathways, increased viral replication and virus load, gradual loss of peripheral CD4+T cells and depletion of T lymphocytes at mucosal sites that collectively lead to progressive immune deficiency and AIDS development. T cells derived from HIV patients were anergic and failed to mount a robust adaptive immune response. The host, on the other hand, becomes vulnerable to opportunistic infections such as tuberculosis and AIDS-related cancer such as Kaposi sarcoma, non-Hodgkin lymphoma, and cervical cancer with remarkable level of immunosuppression. Elucidation of the various mechanisms involved in these immunologic perturbations is necessary to understand HIV pathogenesis for an effective immunotherapy.
Highlights
Background and SignificanceInfection with human immunodeficiency virus (HIV) has been identified as a causal agent of AIDS, a pandemic disease that constitutes a global public health threat for the past 3 decades [1]
The resulting immune dysfunction in HIV patients is likely due to combinatorial effects resulting from infection of immune cells (CD4+T cells, macrophages, dendritic cells) with HIV, uncontrolled viral replication that impairs antigen presentation, increased mutations in env protein gp120 that leads to virus tropism and survival, increased activation of T helper cells by alloantigens, increased apoptosis by activated CD4+T helper cells, down-regulation of CD4+synthesis with functional impairment, and perturbation of cytokine pathways [4,5,6]
HIV is a relentlessly progressive disease and difficult to cure with highly active antiretroviral therapy (HAART) due to the persistence of HIV-1 virus in latent reservoirs that may lead to viral remission and development of AIDS [9]
Summary
Background and SignificanceInfection with human immunodeficiency virus (HIV) has been identified as a causal agent of AIDS, a pandemic disease that constitutes a global public health threat for the past 3 decades [1]. The progressive death of T lymphocytes is attributed to immune activation rather than to viral cytopathic effect.
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