Viral load of SARS-CoV-2 Omicron BA.5 is lower than that of BA.2 despite the higher infectivity of BA.5.

BA.5 COVID-19 Omicron variant SARS-CoV-2 viral load

Journal

Immunity, inflammation and disease
ISSN: 2050-4527
Titre abrégé: Immun Inflamm Dis
Pays: England
ID NLM: 101635460

Informations de publication

Date de publication:
Feb 2023
Historique:
revised: 25 01 2023
received: 08 12 2022
accepted: 30 01 2023
entrez: 25 2 2023
pubmed: 26 2 2023
medline: 3 3 2023
Statut: ppublish

Résumé

Sublineage BA.5 of the SARS-CoV-2 Omicron variant rapidly spread and replaced BA.2 in July 2022 in Tokyo. A high viral load can be a possible cause of high transmissibility. The copy numbers of SARS-CoV-2 in nasopharyngeal swab samples obtained from all patients visiting the hospital where this research was conducted were measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Viral genotypes were determined using PCR-based melting curve analysis. Next, whole-genome sequencing was performed using approximately one fifth of the samples to verify the viral genotypes determined using PCR. Then, the copy numbers of the BA.1, BA.2, and BA.5 cases were compared. Contrary to expectations, the copy numbers of the BA.5 cases (median 4.7 × 10 The results presented here suggest that the increased infectivity of BA.5 is not caused by higher viral loads, but presumably by other factors such as increased affinity to human cell receptors or immune escape due to its L452R mutation.

Sections du résumé

BACKGROUND BACKGROUND
Sublineage BA.5 of the SARS-CoV-2 Omicron variant rapidly spread and replaced BA.2 in July 2022 in Tokyo. A high viral load can be a possible cause of high transmissibility.
METHODS AND RESULTS RESULTS
The copy numbers of SARS-CoV-2 in nasopharyngeal swab samples obtained from all patients visiting the hospital where this research was conducted were measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Viral genotypes were determined using PCR-based melting curve analysis. Next, whole-genome sequencing was performed using approximately one fifth of the samples to verify the viral genotypes determined using PCR. Then, the copy numbers of the BA.1, BA.2, and BA.5 cases were compared. Contrary to expectations, the copy numbers of the BA.5 cases (median 4.7 × 10
CONCLUSION CONCLUSIONS
The results presented here suggest that the increased infectivity of BA.5 is not caused by higher viral loads, but presumably by other factors such as increased affinity to human cell receptors or immune escape due to its L452R mutation.

Identifiants

pubmed: 36840495
doi: 10.1002/iid3.783
pmc: PMC9933202
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e783

Subventions

Organisme : JST-CREST
ID : JPMJCR20H2
Organisme : Japan Agency for Medical Research and Development
ID : 20nk0101612h0901

Informations de copyright

© 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.

Références

Cell. 2022 Jul 7;185(14):2422-2433.e13
pubmed: 35772405
Med (N Y). 2022 Sep 9;3(9):636-643.e4
pubmed: 35981541
Science. 2022 Aug 19;377(6608):890-894
pubmed: 35857529
J Med Virol. 2022 Nov;94(11):5543-5546
pubmed: 35790476
Nat Rev Microbiol. 2023 Mar;21(3):147-161
pubmed: 36460930
Nat Med. 2022 Sep;28(9):1785-1790
pubmed: 35760080
N Engl J Med. 2022 Jul 7;387(1):86-88
pubmed: 35731894
Lancet Microbe. 2022 Dec;3(12):e898
pubmed: 35963276

Auteurs

Yuna Takatsuki (Y)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Yuta Takahashi (Y)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Jun Nakajima (J)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Yumi Iwasaki (Y)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Katsutoshi Nagano (K)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Chihiro Tani-Sassa (C)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Sonoka Yuasa (S)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Saki Kanehira (S)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Kazunari Sonobe (K)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Yoko Nukui (Y)

Infection Control and Prevention, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Hiroaki Takeuchi (H)

Department of Molecular Virology, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Kousuke Tanimoto (K)

Genome Laboratory, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Research Core, Institute of Research, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Yukie Tanaka (Y)

Department of Molecular Microbiology, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Akinori Kimura (A)

Institute of Research, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Naoya Ichimura (N)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

Shuji Tohda (S)

Clinical Laboratory, Tokyo Medical and Dental University (TMDU) Hospital, Tokyo, Japan.

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Classifications MeSH