SARS-CoV and SARS-Cov-2: All You Need to Know

SARS-CoV

SARS‐CoV (causative pathogen of Severe Acute Respiratory Syndrome or SARS) and SARS‐CoV‐2 (causative pathogen of Coronavirus Disease 2019 or COVID‐19) are positive‐sense RNA viruses belonging to the family of Coronaviridae, able to cause severe respiratory diseases.1  

Many people are wondering why the responses to and the outcomes for the SARS-CoV viruses has been so different.

SARS originated in China’s Guangdong province on November 27, 2002. It presented as a respiratory disease caused by the SARS coronavirus (SARSCoV).2   At that time doctors noted that they observed an unusual pneumonia. However, the disease was not reported to the World Health Organization at that time. 

In February of 2003, another outbreak occurred in Hanoi, Vietnam, and a WHO officer, who later died, examined a patient there and reported a large outbreak to the WHO main office on March 10, 2003.

Meanwhile, a doctor from Guangdong province traveled to Hong Kong and stayed at the Metropol Hotel along with a number of other international travelers. The doctor was infected with what we now know as SARS-CoV-1. The virus was transmitted to at least a dozen other hotel guests. Two returned to Canada and took the virus there. One returned to Ireland, one to the United States. Three went to Singapore, and one to Vietnam. In addition, a few people were hospitalized in Hong Kong, leading to an outbreak in the hospital there. 

From that point, SARS spread to much of the world, although most cases remained in Asia. The virus was aggressive and lethal. Patients typically showed symptoms within two to three days. There were few reports of any infections without symptoms. Masks were worn, temperature scanners were placed in all major public gathering places in China and other parts of Asia, and quarantines were implemented. The virus infection peaked in late May of 2003 and then it disappeared. By July 2003, the WHO declared the threat over. The infection affected 8422 individuals leading to 916 deaths and a casefatality ratio of 10.9% across 29 countries. The pandemic cost the global economy an estimated $30 billion to $100 billion.1

SARS-CoV demonstrated that animal strains of SARS-CoV could jump the species barrier, thereby expanding perception of pandemic threats.3

SARS cases were more severe, in general. It’s estimated that 20 to 30 percent of people with SARS required mechanical ventilation.4 Common symptoms of SARS included fever, cough, dyspnea, and occasionally watery diarrhea. Of infected patients 10% died, with higher fatality rates in older patients and those with medical comorbidities. Human-to-human transmission was documented, mostly in health care settings.5 

The early symptoms of SARS and COVID19 are very similar, including fever, cough, headache, shortness breath and breathing difficulties. Diarrhea was reported in about 2025% of patients with SARS, while intestinal symptoms were not as widely described in patients with COVID19. In addition, most patients with SARS and COVID19 developed lymphopenia with highlevels of proinflammatory cytokines including interleukin (IL)1b and IL6.6

There are other similarities of these viruses, for example:

  • are respiratory illnesses caused by coronaviruses
  • are spread by respiratory droplets produced when a person with the virus coughs or sneezes, or by contact with contaminated objects or surfaces
  • have similar stability in the air and on various surfaces
  • can lead to potentially serious illness, sometimes requiring oxygen or mechanical ventilation. 
  • can have worsening symptoms later on in the illness
  • have similar at-risk groups, such as older adults and those with underlying health conditions

With so much in common why was COVID-19 not contained in the same way with the same outcomes? As more is learned about this virus many speculate that the answers lie in the differences between the two. 

COVID-19 appears to transmit much more easily than SARS. One possible explanation is that the amount of virus, or viral load, appears to be highest in the nose and throat of people with COVID-19 shortly after symptoms develop. This is in contrast to SARS, in which viral loads peaked much later in the illness. This indicates that people with COVID-19 may be transmitting the virus earlier in the course of the infection, just as their symptoms are developing, but before they begin to worsen. According to the Centers for Disease Control and Prevention (CDC), some research suggests that COVID-19 is spread by people who are not showing any symptoms. This is in contrast to SARS, which has no reported cases of transmission before symptoms develop.

A study compared the specific area of the viral protein that’s responsible for binding to the host cell receptor. It observed that the receptor binding site of COVID-19 binds to the host cell receptor with a higher affinity than that of SARS.  If the new coronavirus indeed has a higher binding affinity for its host cell receptor, this could also explain why it appears to spread more easily than the SARS virus.7

It has also been found that people with COVID-19 appear to shed the virus earlier in the course of their infection than people with SARS. This makes it more difficult to detect who has the virus and isolate them before they spread it to others.

We are also seeing a difference in the need for vaccines. Vaccine studies for SARS-CoV-1 were started and tested in animal models. An inactivated whole virus was used in ferrets, nonhuman primates and mice. All of the vaccines resulted in protective immunity, but there were complications; the vaccines resulted in an immune disease in animals. No human studies were done, nor were the vaccine studies taken further because the virus disappeared. Many factors may have been involved in the end of SARS-CoV-1: summer weather, a strict quarantine of all those who had contact with infected individuals, etc however we don’t really know why the epidemic ended.

It appears there is a need for a vaccine for COVID-19 in order to end the pandemic. As I write this some healthcare providers have received it and other shipments are on their way. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, offered a timeline for ending the COVID-19 pandemic this week, saying that if the coming vaccination campaign goes well we could approach herd immunity by summer’s end and “normality that is close to where we were before” by the end of 2021.

References

  1. Conforti C, Giuffrida R, Dianzani C, Di Meo N, Zalaudek I. COVID‐19 and psoriasis: is it time to limit treatment with immunosuppressants? A call for action. Dermatol Ther. 2020. Mar;11:e13298 10.1111/dth.13298.
  2. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID‐19 and potential vaccines: lessons learned from SARS and MERS epidemicAsian Pac J Allergy Immunol. 2020;38:1‐9. 10.12932/AP-200220-0772.
  3. de Wilde  AH, Snijder  EJ, Kikkert  M, van Hemert  MJ.  Host factors in coronavirus replication.  Curr Top Microbiol Immunol. 2018;419:1-42. doi:10.1007/82_2017_25
  4. Paules CI, Marston HD, Fauci AS. Coronavirus Infections—More Than Just the Common Cold. JAMA.2020;323(8):707–708. doi:10.1001/jama.2020.0757
  5. Paules CI, Marston HD, Fauci AS. Coronavirus Infections—More Than Just the Common Cold. JAMA.2020;323(8):707–708. doi:10.1001/jama.2020.0757
  6. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID‐19 and potential vaccines: lessons learned from SARS and MERS epidemicAsian Pac J Allergy Immunol. 2020;38:1‐9. 10.12932/AP-200220-0772.
  7. Tai, W., He, L., Zhang, X. et al. Characterization of the receptor-binding domain (RBD) of 2019 novel coronavirus: implication for development of RBD protein as a viral attachment inhibitor and vaccine. Cell Mol Immunol 17, 613–620 (2020). https://doi.org/10.1038/s41423-020-0400-4

 

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