4.7 Article

Viral load of SARS-CoV-2 Omicron is not high despite its high infectivity

期刊

JOURNAL OF MEDICAL VIROLOGY
卷 94, 期 11, 页码 5543-5546

出版社

WILEY
DOI: 10.1002/jmv.27974

关键词

COVID-19; Delta variant; melting curve analysis; Omicron variant; SARS-CoV-2; viral load

类别

资金

  1. JST-CREST [JPMJCR20H2]
  2. Japan Agency for Medical Research and Development [20nk0101612h0901]

向作者/读者索取更多资源

The Omicron variant of COVID-19 has spread rapidly worldwide, surpassing the speed of the Delta variant. However, this increased transmissibility is not due to higher viral loads. The study suggests that factors such as increased affinity to cell receptors or immune escape may contribute to the enhanced infectivity of the Omicron variant.
Patients infected with the Omicron variant of severe acute respiratory syndrome coronavirus 2 has increased worldwide since the beginning of 2022 and the variant has spread more rapidly than the Delta variant, which spread in the summer of 2021. It is important to clarify the cause of the strong transmissibility of the Omicron variant to control its spread. In 694 patients with coronavirus disease 2019, the copy numbers of virus in nasopharyngeal swab-soaked samples and the viral genotypes were examined using quantitative polymerase chain reaction (PCR) and PCR-based melting curve analysis, respectively. Whole-genome sequencing was also performed to verify the viral genotyping data. There was no significant difference (p = 0.052) in the copy numbers between the Delta variant cases (median 1.5 x 10(5) copies/mu l, n = 174) and Omicron variant cases (median 1.2 x 10(5) copies/mu l, n = 328). During this study, Omicron BA.1 cases (median 1.1 x10(5) copies/mu l, n = 275) began to be replaced by BA.2 cases (median 2.3 x 10(5) copies/mu l, n = 53), and there was no significant difference between the two groups (p = 0.33). Our results suggest that increased infectivity of the Omicron variant and its derivative BA.2 is not caused by higher viral loads but by other factors, such as increased affinity to cell receptors or immune escape.

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