RESUMO
COVID-19 pandemic caused by SARS-CoV-2 infection severely threatens global health and economic development. No effective antiviral drug is currently available to treat COVID-19 and any other human coronavirus infections. We report herein that a macrolide antibiotic, carrimycin, potently inhibited the cytopathic effects (CPE) and reduced the levels of viral protein and RNA in multiple cell types infected by human coronavirus 229E, OC43, and SARS-CoV-2. Time-of-addition and pseudotype virus infection studies indicated that carrimycin inhibited one or multiple post-entry replication events of human coronavirus infection. In support of this notion, metabolic labelling studies showed that carrimycin significantly inhibited the synthesis of viral RNA. Our studies thus strongly suggest that carrimycin is an antiviral agent against a broad-spectrum of human coronaviruses and its therapeutic efficacy to COVID-19 is currently under clinical investigation.
RESUMO
Human coronavirus OC43 (HCoV-OC43) and severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) belong to the β-coronavirus genus. Since the discovery in 1967, HCoV-OC43 has been continuously circulating in human population and has become one of the common seasonal respiratory viruses. SARS-CoV-2, which has a higher morbidity and fatality rate, appeared at the end of 2019, followed by the emergence of a variety of variants, and the transmission and infection capacity of SARS-CoV-2 has been enhanced. HCoV-OC43 may be similar to SARS-CoV-2 in terms of genomic structure and function, species evolution, epidemic characteristics and clinical manifestations. In this review, the epidemiology, genomics, phylogenetic evolution and other aspects of HCoV-OC43 and SARS-CoV-2 were analyzed. Such an analysis would be helpful to understand the association and differences between the two viruses, and provide reference for understanding the potential threats of HCoV-OC43.
RESUMO
Objective@#In this study, we tested for the presence of four human coronaviruses (HCoVs) in children with respiratory tract disease in Fuzhou, Fujian, China.@*Methods@#Nasopharyngeal aspirates were collected from children with respiratory tract disease from Nov, 2007 to Jan, 2015. A total of 266 clinical samples were tested for HCoVs using reverse-transcription polymerase chain reaction (RT-PCR). The positive products were sequenced and compared with those in GenBank by BLAST. The positive samples were then tested for HCoV-HKU1 and HCoV-NL63 using RT-PCR method . We compared the 440 bp pol gene sequence of the 8 HCoV isolates in Fuzhou, China to other HCoV isolates documented in the GenBank database by using MEGA software version 6.06 and the neighbor-joining method .@*Results@#HCoVs were detected in 8 patients (3.0%) out of the 266 children. Two of 266 (0.38%) were positive for HCoV-HKU1; 1 of 266(0.38%)were positive for HCoV-NL63; 1 of 266 (0.38%) were positive for HCoV-229E; 4 of 266 (1.5%)were positive for HCoV-OC43. All of children who were positive for HCoV had respiratory illness. Two HCoV-HKU1 were found to co-infect with human parainfluenza virus type 3 (HPIV-3). The 8 HCoV strains in our study fell into four clusters. Two strains of HCoV-HKU1 were genotype A.@*Conclusions@#HCoV infections were probably associated with upper and lower respiratory illness in children. Additional studies are needed to investigate the potential roles of these HCoVs in diseases.
RESUMO
Severe acute respiratory syndrome (SARS) is a life-threatening disease for which accurate diagnosis is essential. Although many tools have been developed for the diagnosis of SARS, false-positive reactions in negative sera may occur because of cross-reactivity with other coronaviruses. We have raised polyclonal and monoclonal antibodies (Abs) using a recombinant form of the SARS virus nucleocapsid protein. Cross-reactivity of these anti-SARS Abs against human coronavirus (HCoV) 229E and HCoV OC43 were determined by Western blotting. The Abs produced reacted with recombinant SARS virus nucleocapsid protein, but not with HCoV 229E or HCoV OC43.