COVID-19 and SARS-CoV-2 viral load

COVID-19 and SARS-CoV-2 viral load

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There has been a bit of discussion recently about the importance of viral load in the transmission and pathogenesis of COVID-19. Until the infectious dose of the SARS-CoV-2 virus has been determined, our understanding of the contribution of viral load to disease dynamics will be speculative.

Methods of measuring the amount of virus in patients are relatively crude. Nevertheless, there has been a small study of viral dynamics in mild and severe COVID-19 that support increasing viral load as infection progresses [1]. Higher figures were recorded in severe infections. But note; the measurement was based on SARS-CoV-2 viral RNA detection in a small cases series. Other studies have failed to demonstrate a correlation between viral load and severity, so the jury is still out on the issue. In another recent study, higher viral loads were found in the nose than in the throat and peaked around 10 days [2].

The reason viral load has come under scrutiny is that higher amounts of some other viruses that cause respiratory infection are known to increase the risk of transmission and increase disease severity [3]. Infectivity and severity are two different issues. Once established, the consequences of viral infection do not necessarily depend on the amount of virus involved at the initial encounter.

Disease severity in COVID-19 spans an extreme range from death due to acute respiratory distress syndrome, thrugh mild illness, to a complete lack of symptoms. In patients who recover from a mild illness, acquired immunity takes over control of the infection to help restore normality, while patients with more severe disease do not engage their acquired immunity until after their innate immunity goes into overdrive to cause a bystander effect [4]. Opinion is divided on whether this process is mainly due to viral features or to specific patient characteristics. Either way, the contribution of viral load is unclear.

From the limited evidence available, and experience with other coronaviruses, patients with severe disease need to be considered a high risk to those close to them, whether household contacts, carers or healthcare workers. But if high viral loads can be detected in asymptomatic infection, we may need to reconsider the load/severity concept [5]. Other aspects of encounter with SARS-CoV-2 have to be taken into account before we can develop a fuller concept of infectivity that goes beyond detectability.

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See also COVID-19, a reader, COVID 5 facts

References

  1. Liu Y, Yan LM, Wan L, Xiang TX, Le A, et al. Viral dynamics in mild and severe cases of COVID-19. Lancet Infect Dis. 2020 Mar 19. pii: S1473-3099(20)30232-2. doi: 10.1016/S1473-3099(20)30232-2.
  2. Zou L, Ruan F, Huang M, Liang L, Huang H, et al. SARS-CoV-2 Viral Load in Upper Respiratory Specimens of Infected Patients. N Engl J Med. 2020 Mar 19; 382(12):1177-1179. doi: 10.1056/NEJMc2001737.
  3. Granados A, Peci A, McGeer A, Gubbay JB. Influenza and rhinovirus viral load and disease severity in upper respiratory tract infections. J Clin Virol. 2017 Jan; 86:14-19. doi: 10.1016/j.jcv.2016.11.008.
  4. Channappanavar R, Perlman S. Pathogenic human coronavirus infections: causes and consequences of cytokine storm and immunopathology. Semin Immunopathol. 2017 Jul;39(5):529-539. doi: 10.1007/s00281-017-0629-x
  5. Kim ES, Chin BS, Kang CK, Kim NJ, Kang YM, et al.; Korea National Committee for Clinical Management of COVID-19. Clinical Course and Outcomes of Patients with Severe Acute Respiratory Syndrome Coronavirus 2 Infection: a Preliminary Report of the First 28 Patients from the Korean Cohort Study on COVID-19. J Korean Med Sci. 2020 Apr 6; 35(13):e142. doi: 10.3346/jkms.2020.35.e142.

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