The rapid spread of the Delta variant of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) became a serious concern worldwide in summer 2021. We examined the copy number and variant types of all SARS‐CoV‐2‐positive patients who visited our hospital from February to August 2021 using polymerase chain reaction (PCR) tests. Whole genome sequencing was performed for some samples. The R.1 variant (B.1.1.316) was responsible for most infections in March, replacing the previous variant (B.1.1.214); the Alpha (B.1.1.7) variant caused most infections in April and May; and the Delta variant (B.1.617.2) was the most prevalent in July and August. There was no significant difference in the copy numbers among the previous variant cases (n = 29, median 3.0 × 104 copies/µl), R.1 variant cases (n = 28, 2.1 × 105 copies/µl), Alpha variant cases (n = 125, 4.1 × 105 copies/µl), and Delta variant cases (n = 106, 2.4 × 105 copies/µl). Patients with Delta variant infection were significantly younger than those infected with R.1 and the previous variants, possibly because many elderly individuals in Tokyo were vaccinated between May and August. There was no significant difference in mortality among the four groups. Our results suggest that the increased infectivity of Delta variant may be caused by factors other than the higher viral loads. Clarifying these factors is important to control the spread of Delta variant infection.

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 × 10 5 copies/μl, n = 174) and Omicron variant cases (median 1.2 × 10 5 copies/μl, n = 328). During this study, Omicron BA.1 cases (median 1.1 ×10 5 copies/μl, n = 275) began to be replaced by BA.2 cases (median 2.3 × 10 5 copies/μl, 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.

The rapid spread of the Delta variant of SARS-CoV-2 became a serious concern worldwide in summer 2021. We examined the copy number and variant types of all SARS-CoV-2-positive patients who visited our hospital from February to August 2021 using PCR tests. Whole genome sequencing was performed for some samples. The R.1 variant (B.1.1.316) was responsible for most infections in March, replacing the previous variant (B.1.1.214); the Alpha (B.1.1.7) variant caused most infections in April and May; and the Delta variant (B.1.617.2) was the most prevalent in July and August. There was no significant difference in copy numbers among the previous variant cases (n=29, median 3.0x104 copies/μL), R.1 variant cases (n=28, 2.1x105 copies/μL), Alpha variant cases (n=125, 4.1x105 copies/μL), and Delta variant cases (n=106, 2.4x105 copies/μL). Patients with Delta variant infection were significantly younger than those infected with R.1 and the previous variants, possibly because many elderly individuals in Tokyo were vaccinated between May and August. There was no significant difference in mortality among the four groups. Our results suggest that the increased infectivity of Delta variant may be caused by factors other than the higher viral loads. Clarifying these factors is important to control the spread of Delta variant infection.

The spread of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) variants, such as B.1.1.7 and B.1.351, has become a crucial issue worldwide. Therefore, we began testing all patients with COVID‐19 for the N501Y and E484K mutations by using polymerase chain reaction (PCR)‐based methods. Nasopharyngeal swab samples from 108 patients who visited our hospital between February and April 2021 were analyzed. The samples were analyzed using reverse transcription‐PCR with melting curve analysis to detect the N501Y and E484K mutations. A part of the samples was also subjected to whole‐genome sequencing (WGS). Clinical parameters such as mortality and admission to the intensive care unit were analyzed to examine the association between increased disease severity and the E484K mutation. The ratio of cases showing the 501N + 484K mutation rapidly increased from 8% in February to 46% in March. WGS revealed that the viruses with 501N + 484K mutation are R.1 lineage variants. Evidence of increased disease severity related to the R.1 variants was not found. We found that the R.1 lineage variants rapidly prevailed in Tokyo in March 2021, which suggests the increased transmissibility of R.1 variants, while they showed no increased severity.

Background: The spread of SARS-CoV-2 variants, such as B.1.1.7 and B.1.351, has become a crucial issue worldwide. Therefore, we began testing all patients with COVID-19 for the N501Y and E484K mutations associated with SARS-CoV-2. Study design: Nasopharyngeal swab samples from 108 patients who visited our hospital between February and April 2021 were analyzed. The samples were analyzed using reverse transcription-polymerase chain reaction with melting curve analysis to detect the N501Y and E484K mutations. A part of the samples were also subjected to whole genome sequencing. Clinical parameters such as mortality and admission to the intensive care unit were analyzed to examine the association between increased disease severity and the E484K mutation. Results: The ratio of cases showing the 501N+484K mutation rapidly increased from 8% in February to 46% in March. Whole genome sequencing revealed that the viruses with 501N+484K mutation are R.1 lineage variants. Evidence of increased disease severity related to the R.1 variants were not found. Conclusions: We found that the R.1 lineage variants rapidly prevailed in Tokyo in March 2021.

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 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 4 copies/μL, n = 291) were significantly ( p = .001) lower than those of BA.2 cases (median 1.1 × 10 5 copies/μL, n = 184). There was no significant difference ( p = .44) between the BA.5 and BA.1 cases (median, 3.3 × 10 4 copies/μL; n = 215). Conclusion: 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.

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. Therefore, 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 quantitative polymerase chain reaction (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 X 104copies/uL, n = 290) were significantly (p = 0.001) lower than those of BA.2 cases (median 1.1 X 105copies/uL, n = 184). There was no significant difference between the BA.5 and BA.1 cases (median, 3.1 X 104copies/uL; n = 215). 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.