PMID- 33841434
OWN - NLM
STAT- MEDLINE
DCOM- 20210419
LR  - 20210419
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 12
DP  - 2021
TI  - COVID-19 and HIV-Associated Immune Reconstitution Inflammatory Syndrome: 
      Emergence of Pathogen-Specific Immune Responses Adding Fuel to the Fire.
PG  - 649567
LID - 10.3389/fimmu.2021.649567 [doi]
LID - 649567
AB  - Both coronavirus disease 2019 (COVID-19) and mycobacterial immune reconstitution 
      inflammatory syndrome (IRIS) in patients with HIV-1 infection result from 
      immunopathology that is characterized by increased production of multiple 
      pro-inflammatory chemokines and cytokines associated with activation of myeloid 
      cells (monocytes, macrophages and neutrophils). We propose that both conditions 
      arise because innate immune responses generated in the absence of effective 
      adaptive immune responses lead to monocyte/macrophage activation that is 
      amplified by the emergence of a pathogen-specific adaptive immune response skewed 
      towards monocyte/macrophage activating activity by the immunomodulatory effects 
      of cytokines produced during the innate response, particularly interleukin-18. In 
      mycobacterial IRIS, that disease-enhancing immune response is dominated by a Th1 
      CD4(+) T cell response against mycobacterial antigens. By analogy, it is proposed 
      that in severe COVID-19, amplification of monocyte/macrophage activation results 
      from the effects of a SARS-CoV-2 spike protein antibody response with 
      pro-inflammatory characteristics, including high proportions of IgG3 and IgA2 
      antibodies and afucosylation of IgG1 antibodies, that arises from B cell 
      differentiation in an extra-follicular pathway promoted by activation of 
      mucosa-associated invariant T cells. We suggest that therapy for the 
      hyperinflammation underlying both COVID-19 and mycobacterial IRIS might be 
      improved by targeting the immunomodulatory as well as the pro-inflammatory 
      effects of the 'cytokine storm'.
CI  - Copyright (c) 2021 Seddiki and French.
FAU - Seddiki, Nabila
AU  - Seddiki N
AD  - Inserm, U955, Equipe 16, Creteil, 94000, France, Universite Paris Est, Faculte de 
      Medecine, Creteil, France.
AD  - Vaccine Research Institute (VRI), Creteil, France.
FAU - French, Martyn
AU  - French M
AD  - School of Biomedical Sciences, University of Western Australia, Perth, WA, 
      Australia.
AD  - Division of Immunology, PathWest Laboratory Medicine, Perth, WA, Australia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20210324
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (Spike Glycoprotein, Coronavirus)
RN  - 0 (spike protein, SARS-CoV-2)
SB  - IM
MH  - COVID-19/*immunology
MH  - HIV Infections/*immunology
MH  - HIV-1/*immunology
MH  - Humans
MH  - Immune Reconstitution Inflammatory Syndrome/*immunology
MH  - Immunity, Innate
MH  - Macrophage Activation
MH  - Macrophages/immunology
MH  - Monocytes/immunology
MH  - SARS-CoV-2/*immunology
MH  - Spike Glycoprotein, Coronavirus/immunology
MH  - Th1 Cells/immunology
PMC - PMC8024517
OTO - NOTNLM
OT  - COVID-19
OT  - SARS-CoV-2
OT  - human immunodeficiency virus type 1
OT  - immune reconstitution inflammatory syndrome
OT  - interleukin-18
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/04/13 06:00
MHDA- 2021/04/20 06:00
PMCR- 2021/03/24
CRDT- 2021/04/12 06:17
PHST- 2021/01/05 00:00 [received]
PHST- 2021/03/08 00:00 [accepted]
PHST- 2021/04/12 06:17 [entrez]
PHST- 2021/04/13 06:00 [pubmed]
PHST- 2021/04/20 06:00 [medline]
PHST- 2021/03/24 00:00 [pmc-release]
AID - 10.3389/fimmu.2021.649567 [doi]
PST - epublish
SO  - Front Immunol. 2021 Mar 24;12:649567. doi: 10.3389/fimmu.2021.649567. eCollection 
      2021.