Mutations, deletions and recombination breakpoints in the stem-loop II motif (s2m) of Australian severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) isolates Panel A: Deletions and mutations in the primary, secondary and tertiary structures of the coronavirus disease 2019 (COVID-19) s2m RNA genetic element based on the three-dimensional crystal structure of the SARS virus. Conventional RNA helical base pairings are indicated in italics. Sequence complements are indicated using colour-coded brackets. The G19 mutation (arrowhead) of the Australian SARS-CoV-2 is shown with purple colour. Asterisks label the RNA recombination breakpoints based on analysis of 1319 Australia SARS-CoV-2 sequences using Recco algorithm (https://recco.bioinf.mpi-inf.mpg.de/) (P < 0.002). Panel B: Schematic representation of the s2m RNA secondary structure of the SARS virus, with tertiary structural interactions indicated as long range contacts. 4 ◆ Letter MJA 2020 1.e1
Objective
To examine transmission and evolution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in shipboard quarantine of the Diamond Princess cruise ship.
Methods
We obtained the full SARS-CoV-2 genome sequences of 28 samples from the Global Initiative on Sharing All Influenza Data database. The samples were collected between 10 and 25 February 2020 and came for individuals who had been tested for SARS-CoV-2 during the quarantine on the cruise ship. These samples were later sequenced in either Japan or the United States of America. We analysed evolution dynamics of SARS-CoV-2 using computational tools of phylogenetics, natural selection pressure and genetic linkage.
Findings
The SARS-CoV-2 outbreak in the cruise most likely originated from either a single person infected with a virus variant identical to the WIV04 isolates, or simultaneously with another primary case infected with a virus containing the 11083G > T mutation. We identified a total of 24 new viral mutations across 64.2% (18/28) of samples, and the virus evolved into at least five subgroups. Increased positive selection of SARS-CoV-2 were statistically significant during the quarantine (Tajima’s
D
: −2.03,
P
< 0.01; Fu and Li’s
D
: −2.66,
P
< 0.01; and Zeng’s
E
: −2.37,
P
< 0.01). Linkage disequilibrium analysis confirmed that ribonucleic acid (RNA) recombination with the11083G > T mutation also contributed to the increase of mutations among the viral progeny.
Conclusion
The findings indicate that the 11083G > T mutation of SARS-CoV-2 spread during shipboard quarantine and arose through
de novo
RNA recombination under positive selection pressure.
Public distrust has undermined COVID-19 vaccine acceptance and has become a major public health issue in the battle against SARS-CoV-2 transmission globally. Here we present the first evidence that the vaccination coverage rate is inversely correlated to the mutation frequency of the SARS-CoV-2 delta variant in 16 countries (R2=0.878), strongly indicating that full vaccination against COVID-19 is critical to suppress emergent mutations. We also present a promising tool to forecast new COVID-19 outbreaks. The Tajima D test, an evolutionary algorithm, with a threshold value of -2.50 is shown to be an accurate predictor of new outbreaks. We recommend that universal vaccination, as well as mitigation strategies, and genomic surveillance continue to be employed to prevent further viral transmission.
Here we report the first evidence of recombination of monkeypox genome in natural transmission by analyzing six tandem repeats (TRs) among 415 sequences collected between January to July 2022. The 2022 monkeypox viral population has diverged into 11 subgroups based on various TRs and their copy numbers. Here we identify 8 new recombinants (six from Slovenia, one from Australia, one from Italy). Our results indicate that the monkeypox genome is evolving and expanding quickly during the 2022 pandemic (Zeng E = -1.65, Achaz Y=-2.52, p< 0.001). We conclude that, In combination with genomic surveillance, TR analysis is a useful tool to monitor and track phylogenetic dynamics of monkeypox transmission.
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