PMID- 32810867
OWN - NLM
STAT- MEDLINE
DCOM- 20210414
LR  - 20231112
IS  - 1477-4054 (Electronic)
IS  - 1467-5463 (Print)
IS  - 1467-5463 (Linking)
VI  - 22
IP  - 2
DP  - 2021 Mar 22
TI  - The Cellular basis of loss of smell in 2019-nCoV-infected individuals.
PG  - 873-881
LID - 10.1093/bib/bbaa168 [doi]
LID - bbaa168
AB  - A prominent clinical symptom of 2019-novel coronavirus (nCoV) infection is 
      hyposmia/anosmia (decrease or loss of sense of smell), along with general 
      symptoms such as fatigue, shortness of breath, fever and cough. The identity of 
      the cell lineages that underpin the infection-associated loss of olfaction could 
      be critical for the clinical management of 2019-nCoV-infected individuals. Recent 
      research has confirmed the role of angiotensin-converting enzyme 2 (ACE2) and 
      transmembrane protease serine 2 (TMPRSS2) as key host-specific cellular moieties 
      responsible for the cellular entry of the virus. Accordingly, the ongoing medical 
      examinations and the autopsy reports of the deceased individuals indicate that 
      organs/tissues with high expression levels of ACE2, TMPRSS2 and other putative 
      viral entry-associated genes are most vulnerable to the infection. We studied if 
      anosmia in 2019-nCoV-infected individuals can be explained by the expression 
      patterns associated with these host-specific moieties across the known olfactory 
      epithelial cell types, identified from a recently published single-cell 
      expression study. Our findings underscore selective expression of these viral 
      entry-associated genes in a subset of sustentacular cells (SUSs), Bowman's gland 
      cells (BGCs) and stem cells of the olfactory epithelium. Co-expression analysis 
      of ACE2 and TMPRSS2 and protein-protein interaction among the host and viral 
      proteins elected regulatory cytoskeleton protein-enriched SUSs as the most 
      vulnerable cell type of the olfactory epithelium. Furthermore, expression, 
      structural and docking analyses of ACE2 revealed the potential risk of olfactory 
      dysfunction in four additional mammalian species, revealing an evolutionarily 
      conserved infection susceptibility. In summary, our findings provide a plausible 
      cellular basis for the loss of smell in 2019-nCoV-infected patients.
CI  - (c) The Author(s) 2020. Published by Oxford University Press. All rights reserved. 
      For Permissions, please email: journals.permissions@oup.com.
FAU - Gupta, Krishan
AU  - Gupta K
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Mohanty, Sanjay Kumar
AU  - Mohanty SK
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Mittal, Aayushi
AU  - Mittal A
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Kalra, Siddhant
AU  - Kalra S
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Kumar, Suvendu
AU  - Kumar S
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Mishra, Tripti
AU  - Mishra T
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Ahuja, Jatin
AU  - Ahuja J
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Sengupta, Debarka
AU  - Sengupta D
AD  - Indraprastha Institute of Information Technology, Delhi.
FAU - Ahuja, Gaurav
AU  - Ahuja G
AD  - Indraprastha Institute of Information Technology, Delhi.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Brief Bioinform
JT  - Briefings in bioinformatics
JID - 100912837
RN  - 0 (Viral Proteins)
RN  - EC 3.4.17.23 (ACE2 protein, human)
RN  - EC 3.4.17.23 (Angiotensin-Converting Enzyme 2)
SB  - IM
MH  - Angiotensin-Converting Enzyme 2/metabolism
MH  - Anosmia/*pathology
MH  - COVID-19/*complications/pathology/virology
MH  - Humans
MH  - SARS-CoV-2/isolation & purification
MH  - Viral Proteins/metabolism
MH  - Virus Internalization
PMC - PMC7462334
OTO - NOTNLM
OT  - COVID-19
OT  - SARS-CoV-2
OT  - olfaction
OT  - olfactory sensory neurons (OSNs)
OT  - pandemic
OT  - smell
EDAT- 2020/08/19 06:00
MHDA- 2021/04/15 06:00
PMCR- 2020/09/01
CRDT- 2020/08/19 06:00
PHST- 2020/03/30 00:00 [received]
PHST- 2020/06/10 00:00 [revised]
PHST- 2020/07/05 00:00 [accepted]
PHST- 2020/08/19 06:00 [pubmed]
PHST- 2021/04/15 06:00 [medline]
PHST- 2020/08/19 06:00 [entrez]
PHST- 2020/09/01 00:00 [pmc-release]
AID - 5893433 [pii]
AID - bbaa168 [pii]
AID - 10.1093/bib/bbaa168 [doi]
PST - ppublish
SO  - Brief Bioinform. 2021 Mar 22;22(2):873-881. doi: 10.1093/bib/bbaa168.