PMID- 36591299
OWN - NLM
STAT- MEDLINE
DCOM- 20230112
LR  - 20240318
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 13
DP  - 2022
TI  - The relationship between chronic immune response and neurodegenerative damage in 
      long COVID-19.
PG  - 1039427
LID - 10.3389/fimmu.2022.1039427 [doi]
LID - 1039427
AB  - In the past two years, the world has faced the pandemic caused by the severe 
      acute respiratory syndrome 2 coronavirus (SARS-CoV-2), which by August of 2022 
      has infected around 619 million people and caused the death of 6.55 million 
      individuals globally. Although SARS-CoV-2 mainly affects the respiratory tract 
      level, there are several reports, indicating that other organs such as the heart, 
      kidney, pancreas, and brain can also be damaged. A characteristic observed in 
      blood serum samples of patients suffering COVID-19 disease in moderate and severe 
      stages, is a significant increase in proinflammatory cytokines such as 
      interferon-alpha (IFN-alpha), interleukin-1beta (IL-1beta), interleukin-2 (IL-2), interleukin-6 
      (IL-6) and interleukin-18 (IL-18), as well as the presence of autoantibodies 
      against interferon-alpha (IFN-alpha), interferon-lambda (IFN-lambda), C-C motif chemokine ligand 26 
      (CCL26), CXC motif chemokine ligand 12 (CXCL12), family with sequence similarity 
      19 (chemokine (C-C motif)-like) member A4 (FAM19A4), and C-C motif chemokine 
      ligand 1 (CCL1). Interestingly, it has been described that the chronic 
      cytokinemia is related to alterations of blood-brain barrier (BBB) permeability 
      and induction of neurotoxicity. Furthermore, the generation of autoantibodies 
      affects processes such as neurogenesis, neuronal repair, chemotaxis and the 
      optimal microglia function. These observations support the notion that COVID-19 
      patients who survived the disease present neurological sequelae and 
      neuropsychiatric disorders. The goal of this review is to explore the 
      relationship between inflammatory and humoral immune markers and the major 
      neurological damage manifested in post-COVID-19 patients.
CI  - Copyright (c) 2022 Elizalde-Diaz, Miranda-Narvaez, Martinez-Lazcano and 
      Martinez-Martinez.
FAU - Elizalde-Diaz, Jose Pedro
AU  - Elizalde-Diaz JP
AD  - Laboratory of Cell Communication & Extracellular Vesicles, Division of Basic 
      Science, Instituto Nacional de Medicina Genomica, Ciudad de Mexico, Mexico.
FAU - Miranda-Narvaez, Clara Leticia
AU  - Miranda-Narvaez CL
AD  - Laboratorio de Neurofarmacologia Molecular y Nanotecnologia, Instituto Nacional 
      de Neurologia y Neurocirugia Manuel Velasco Suarez, Ciudad de Mexico, Mexico.
FAU - Martinez-Lazcano, Juan Carlos
AU  - Martinez-Lazcano JC
AD  - Laboratorio de Neurofarmacologia Molecular y Nanotecnologia, Instituto Nacional 
      de Neurologia y Neurocirugia Manuel Velasco Suarez, Ciudad de Mexico, Mexico.
FAU - Martinez-Martinez, Eduardo
AU  - Martinez-Martinez E
AD  - Laboratory of Cell Communication & Extracellular Vesicles, Division of Basic 
      Science, Instituto Nacional de Medicina Genomica, Ciudad de Mexico, Mexico.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20221216
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (Chemokines)
RN  - 0 (Interferon-alpha)
RN  - 0 (Interleukin-6)
RN  - 0 (Ligands)
SB  - IM
CIN - Front Immunol. 2023 Jun 01;14:1221642. PMID: 37325637
MH  - Humans
MH  - Chemokines
MH  - COVID-19
MH  - Immunity
MH  - Interferon-alpha
MH  - Interleukin-6
MH  - Ligands
MH  - *Post-Acute COVID-19 Syndrome/complications/immunology/physiopathology
MH  - SARS-CoV-2
MH  - *Neurodegenerative Diseases/etiology/immunology/physiopathology
PMC - PMC9800881
OTO - NOTNLM
OT  - SARS-CoV-2
OT  - autoantigens
OT  - autoantobodies
OT  - inflammatory response
OT  - long COVID syndrome
OT  - neurodegeneration
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- 2023/01/03 06:00
MHDA- 2023/01/04 06:00
PMCR- 2022/12/16
CRDT- 2023/01/02 04:50
PHST- 2022/09/08 00:00 [received]
PHST- 2022/11/28 00:00 [accepted]
PHST- 2023/01/02 04:50 [entrez]
PHST- 2023/01/03 06:00 [pubmed]
PHST- 2023/01/04 06:00 [medline]
PHST- 2022/12/16 00:00 [pmc-release]
AID - 10.3389/fimmu.2022.1039427 [doi]
PST - epublish
SO  - Front Immunol. 2022 Dec 16;13:1039427. doi: 10.3389/fimmu.2022.1039427. 
      eCollection 2022.