The SARS-CoV-2 spike (S) protein, the viral mediator for binding and entry into the host cell, has sparked great interest as a target for vaccine development and treatments with neutralizing antibodies. Initial data suggest that the virus has low mutation rates, but its large genome could facilitate recombination, insertions, and deletions, as has been described in other coronaviruses. Here, we deep-sequenced the complete SARS-CoV-2
S
gene from 18 patients (10 with mild and 8 with severe COVID-19), and found that the virus accumulates deletions upstream and very close to the S1/S2 cleavage site (PRRAR/S), generating a frameshift with appearance of a stop codon. These deletions were found in a small percentage of the viral quasispecies (2.2%) in samples from all the mild and only half the severe COVID-19 patients. Our results suggest that the virus may generate free S1 protein released to the circulation. We suggest that natural selection has favoured a “Don’t burn down the house” strategy, in which free S1 protein may compete with viral particles for the ACE2 receptor, thus reducing the severity of the infection and tissue damage without losing transmission capability.
Aim: Human respiratory syncytial virus (HRSV) is the main cause of respiratory tract infections among infants. Materials & methods: In the present study, the molecular epidemiology of HRSV detected from 2013 to 2017 has been described. Results: A 10% of collected samples were laboratory confirmed for HRSV. Patients under 2 years of age were the main susceptible population to respiratory syncytial virus disease, but an increasingly number of confirmed patients over 65 years of age was reported. Epidemics usually started in autumn and ended in spring. Both HRSV groups co-circulated every season, but the HRSV-B was the most predominant. HRSV-A and HRSV-B strains mainly belonged to ON1 and BA9 genotypes, respectively. Conclusion: The present study reports recent data about the genetic diversity of circulating HRSV in Spain.
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