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Journal of Clinical Infectious Diseases & Practice
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  • Mini Review   
  • J Clin Infect Dis Pract 2023, Vol 8(2): 173

Antagonism of Type I Interferon Early Response and the Increased Risk by HIV and AIDS-Associated Viruses

Shanoon Roff*
Department of Molecular Medicine, Laboratory of Virology Affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Sapienza University, Rome, Italy
*Corresponding Author : Shanoon Roff, Department of Molecular Medicine, Laboratory of Virology Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University, Rome, Italy, Email: Shanoonroff@ez.com

Received Date: Mar 03, 2023 / Published Date: Mar 31, 2023

Abstract

Type I interferon (IFN) response initially limits HIV-1 spread and may delay disease progression by stimulating several immune system components. Nonetheless, persistent exposure to type I IFN in the chronic phase of HIV-1 infection is associated with desensitization and/or detrimental immune activation, thereby hindering immune recovery and fostering viral persistence. This review provides a basis for understanding the complexity and function of IFN pleiotropic activity in HIV-1 infection. In particular, the dichotomous role of the IFN response in HIV-1 immunopathogenesis will be discussed, highlighting recent advances in the dynamic modulation of IFN production in acute versus chronic infection, expression signatures of IFN subtypes, and viral and host factors affecting the magnitude of IFN response during HIV-1 infection. Lastly, the review gives a forward-looking perspective on the interplay between microbiome compositions and IFN response.

Citation: Roff S (2023) Antagonism of Type I Interferon Early Response and the Increased Risk by HIV and AIDS-Associated Viruses. J Clin Infect Dis Pract, 8: 173.

Copyright: © 2023 Roff S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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