Abstract
Human immunodeficiency virus type 1 (HIV-1) infection is a chronic disease without
a known cure. The advent of effective antiretroviral therapy (ART) has enabled people
with HIV (PWH) to have significantly prolonged life expectancies. As a result, morbidity
and mortality associated with HIV-1 infection have declined considerably. However,
these individuals experience chronic systemic inflammation whose multifaceted etiology
is associated with other numerous comorbidities. Inflammasomes are vital mediators
that contribute to inflammatory signaling in HIV-1 infection. Here, we provide an
overview of the inflammatory pathway that underlies HIV-1 infection, explicitly highlighting
the role of the NLRP3 inflammasome. We also delineate the current literature on inflammasomes
and the therapeutic targeting strategies aimed at the NLRP3 inflammasome to moderate
HIV-1 infection-associated inflammation. Here we describe the NLRP3 inflammasome as
a key pathway in developing novel therapeutic targets to block HIV-1 replication and
HIV-1-associated inflammatory signaling. Controlling the inflammatory pathways is
critical in alleviating the morbidities and mortality associated with chronic HIV-1
infection in PWH.
Abbreviations:
HIV (human immunodeficiency virus), SIV (simian immunodeficiency virus), AIDS (acquired immune deficiency syndrome), CCR5 (chemokine receptor 5), CXCR4 (chemokine receptor 4), ART (antiretroviral), PWH (people with HIV), CTL (cytolytic T lymphocytes), Th (T helper), PD-1 (programmed cell death protein 1), LAG-3 (lymphocyte-activation gene 3), TIGIT (T cell immunoreceptor with Ig and ITIM domains), GALT (gut-associated lymphoid tissue), LPS (lipopolysaccharide), HCV (hepatitis C virus), HBV (hepatitis B virus), CMV (cytomegalovirus), PRR (pattern recognition receptor), ASC (apoptosis-associated speck-like protein containing a caspase-recruitment domain), NLR (NOD-like receptors), NACHT (central nucleotide-binding oligomerization), ALR (AIM2-like receptors), AIM2 (absent from melanoma 2), PAMP (pathogen-associated molecular pattern), DAMP (danger-associated molecular patterns)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: July 30, 2022
Accepted:
July 27,
2022
Received in revised form:
July 23,
2022
Received:
June 2,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.
