Journal
CLINICAL INFECTIOUS DISEASES
Volume 72, Issue 12, Pages E978-E992Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/cid/ciaa1747
Keywords
coronavirus; COVID-19; SARS-CoV-2; monoinfection; coinfection; influenza; hamster
Categories
Funding
- National Program on Key Research Project of China [2020YFA0707500, 2020YFA0707504]
- Consultancy Service for Enhancing Laboratory Surveillance of Emerging Infectious Diseases and Research Capability on Antimicrobial Resistance, Department of Health, the Hong Kong Special Administrative Region Government
- High Level-Hospital Program, Health Commission of Guangdong Province, China
- Sanming Project of Medicine in Shenzhen, China [SZSM201911014]
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Simultaneous or sequential coinfection with SARS-CoV-2 and A(H1N1)pdm09 in hamsters resulted in more severe disease than monoinfection, with prior A(H1N1)pdm09 infection lowering SARS-CoV-2 pulmonary viral loads but enhancing lung damage. Suggestions for prevention include whole-population influenza vaccination and early initiation of antiviral treatment using multiplex molecular diagnostics for both viruses.
Background. Clinical outcomes of the interaction between the co-circulating pandemic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and seasonal influenza viruses are unknown. Methods. We established a golden Syrian hamster model coinfected by SARS-CoV-2 and mouse-adapted A(H1N1)pdm09 simultaneously or sequentially. The weight loss, clinical scores, histopathological changes, viral load and titer, and serum neutralizing antibody titer were compared with hamsters challenged by either virus. Results. Coinfected hamsters had more weight loss, more severe lung inflammatory damage, and tissue cytokine/chemokine expression. Lung viral load, infectious virus titers, and virus antigen expression suggested that hamsters were generally more susceptible to SARS-CoV-2 than to A(H1N1)pdm09. Sequential coinfection with A(H1N1)pdm09 one day prior to SARS-CoV-2 exposure resulted in a lower lung SARS-CoV-2 titer and viral load than with SARS-CoV-2 monoinfection, but a higher lung A(H1N1)pdm09 viral load. Coinfection also increased intestinal inflammation with more SARS-CoV-2 nucleoprotein expression in enterocytes. Simultaneous coinfection was associated with delay in resolution of lung damage, lower serum SARS-CoV-2 neutralizing antibody, and longer SARS-CoV-2 shedding in oral swabs compared to that of SARS-CoV-2 monoinfection. Conclusions. Simultaneous or sequential coinfection by SARS-CoV-2 and A(H1N1)pdm09 caused more severe disease than monoinfection by either virus in hamsters. Prior A(H1N1)pdm09 infection lowered SARS-CoV-2 pulmonary viral loads but enhanced lung damage. Whole-population influenza vaccination for prevention of coinfection, and multiplex molecular diagnostics for both viruses to achieve early initiation of antiviral treatment for improvement of clinical outcome should be considered.
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