Severe Acute Respiratory Syndrome (SARS)

The beta coronavirus that causes a severe acute respiratory syndrome, or (SARS) --  is a viral respiratory illness caused by a coronavirus called SARS-associated coronavirus (SARS-CoV). Currently, there is no known SARS transmission anywhere in the world.

SARS-CoV was the first major novel infectious disease to hit the international community in the 21st century. SARS challenged the public health systems of all affected countries, reported a 2009 study.

Now called SARS-COV-1, is a different coronavirus than the SARS-CoV-2, which was identified by the WHO during 2019.

A study published by the NEJM on April 16, 2020, found that the stability of SARS-CoV-2 was similar to that of SARS-CoV-1 under certain circumstances tested. This indicates that differences in the epidemiologic characteristics of these viruses probably arise from other factors, including high viral loads in the upper respiratory tract and the potential for persons infected with SARS-CoV-2 to shed and transmit the virus while asymptomatic.

SARS-CoV Outbreak Timeline

  • 2003 - SARS first reported in Asia in February and became a notifiable disease in China in mid-April. As of July 2003, the WHO reported 325 cases, and the illness spread to about 24 countries in North America, South America, Europe, and Asia during 2003.
  • 2003 - SARS has not re-emerged naturally, but there have been 6 escapes from virology labs: 1 event each in Singapore and Taiwan, and 4 separate escapes of the coronavirus at the same laboratory in Beijing, China.
  • 2004 - The WHO published during October the 'SARS Risk Assessment and Preparedness Framework.' And, the CDC issues “Notice of Embargo of Civets.” A SARS-like virus had been isolated from civets (captured in areas of China where the SARS outbreak originated). CDC banned the importation of civets, which remains in effect.
  • 2005 - A pre-clinical study finds chloroquine is effective in inhibiting the infection and spread of SARS CoV in cell culture. Similar studies describe the role of these proteins in SARS-CoV replication and potential therapeutic strategies aimed at preventing entry of SARS-CoV into target cells.

SARS-CoV Overview

Human coronavirus was initially cultured in the 1960s from nasal cavities of people with the common cold, reports a recent study. They are the 2nd leading cause of the common cold, after rhinoviruses. People around the world commonly get infected with human coronaviruses 229E, NL63, OC43, and HKU1, says the CDC.

There are four main sub-groupings of coronaviruses, known as alpha, beta, gamma, and delta. SARS-CoV is a betacoronavirus, like MERS.

The incubation period for SARS is typically 2 to 7 days, although in some cases it may be as long as 10 days. In a very small proportion of cases, incubation periods of up to 14 days have been reported.

The WHO estimates that the case fatality ratio of SARS ranges from 0% to 50% depending on the age group affected.

SARS-CoV Treatments

A study published in 2015 suggest that convalescent plasma may have a clinically relevant impact in reducing the rate of mortality and viral load in patients with SARI of viral etiology. Post hoc pooled meta-analysis across all viral etiologies showed a statistically significant 75% reduction in the odds of mortality among those who were treated with convalescent plasma or serum. We found no evidence of serious adverse events or complications due to therapy and limited evidence of a reduction in the use of critical care resources and the length of hospital stay.

A study published in 2014 summarized saying 'Convalescent plasma may reduce mortality and appears safe. This therapy should be studied within the context of a well-designed clinical trial or other formal evaluation, including for treatment of Middle East respiratory syndrome coronavirus CoV infection.'

A study published by the NIH in 2006 found the absence of the coronavirus outside the lungs suggests that death is the result of SARS-CoV replicating in the lungs alone. Whether SARS-CoV fatally damages lung tissue directly or whether macrophages recruited to the lungs in response to infection with SARS-CoV cause fatal immunopathological changes remains an open question.

A study published in 2005 found 'all infected healthcare workers whose SARS condition had progressed severely and who had failed to respond to the available treatment, survived after transfusion with convalescent plasma.

SARS-CoV Sources

A 2015 study suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating in bat populations. The results indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin-converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV.

A study published in 2007 found horseshoe bats are the natural reservoir for SARS-CoV-like virus and that civets are the amplification host highlight the importance of wildlife and biosecurity in farms and wet markets, which can serve as the source and amplification centers for emerging infections.

SARS-CoV Gender Differential

To investigate gender differences, during 2019, researchers infected male and female mice of different age groups with SARS-CoV and analyzed their susceptibility to the infection. Our results showed that male mice were more susceptible to SARS-CoV infection compared with age-matched females.

The degree of sex bias to SARS-CoV infection increased with advancing age, such that middle-aged mice showed much more pronounced differences compared with young mice. Enhanced susceptibility of male mice to SARS-CoV was associated with elevated virus titers, enhanced vascular leakage, and alveolar edema. These changes were accompanied by increased accumulation of inflammatory monocyte macrophages and neutrophils in the lungs of male mice, and depletion of inflammatory monocyte macrophages partially protected these mice from lethal SARS. Moreover, the sex-specific differences were independent of T and B cell responses.

Furthermore, ovariectomy or treating female mice with an estrogen receptor antagonist increased mortality, indicating a protective effect for estrogen receptor signaling in mice infected with SARS-CoV. Together, these data suggest that sex differences in the susceptibility to SARS-CoV in mice parallel those observed in patients and also identify estrogen receptor signaling is critical for protection in females.

NOTE: The content on this page is sourced from the CDC, WHO,, and the Precision Vax news network. This information was last fact-checked by healthcare providers, such as Dr. Robert Carlson.