SARS-CoV-2 Coronavirus

During December 2019, the novel coronavirus Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), was identified in China. As the name indicates, the virus is related to the SARS coronavirus (SARS-CoV) that caused a deadly outbreak in 2002-2003.

However, it is not the same virus.

On February 5, 2020, JAMA published a study focused on genetic sequencing data found the SARS-CoV-2 coronavirus shares 79.5% of the genetic sequence with SARS-CoV and has 96.2% homology to a bat coronavirus. In addition, SARS-CoV-2 shares the same cell entry receptor, ACE2, as does SARS-CoV.

On February 11, 2020, the World Health Organization (WHO) announced the official name for the disease associated with SARS-CoV-2, Coronavirus Disease-2019 (COVID-19).

SARS-CoV-2 Coronavirus Origin

The SARS-CoV-2 virus is a betacoronavirus, like MERS-CoV and SARS-CoV, both of which have their origins in bats. The sequences from U.S. patients are similar to those China initially posted, suggesting a recent emergence of this virus from an animal reservoir, such as horseshoe bats (Rhinolophus sinicus).

Extensive virus studies have been conducted at the Wuhan Centers for Disease Control and Prevention (CDC). The identification of multiple SARS-like CoVs in bats has led to the idea that these animals act as hosts of a natural reservoir of these viruses. Although SARS-like viruses have been identified widely in bats in China, viruses identical to SARS-CoV have not yet been documented.

An analysis published in The Lancet sequenced from 9 patients' samples showed that this coronavirus belongs to the subgenus Sarbecovirus. The SARS-CoV-2 virus was more similar to bat-derived coronavirus strains, bat-SL-CoVZC45, and bat-SL-CoVZXC21 than to known human-infecting coronaviruses, including the virus that caused the SARS outbreak of 2003.

"Based on the genome sequence and properties of the virus, there is no basis to suspect the virus was engineered," said Prof. Richard H. Ebright, the laboratory director at the Waksman Institute of Microbiology and a professor of chemistry and chemical biology at Rutgers University.

“Because the bat coronavirus RaTG13 and closely related bat coronaviruses also are known to have been present in a lab," he said, specifically in the coronavirus collection at Wuhan Institute of Virology. 

A February 2020 study published in Nature found a single patient was admitted to the Central Hospital of Wuhan on December 26, 2019. Metagenomic RNA sequencing of a sample of bronchoalveolar lavage fluid from the patient identified a new RNA virus strain from the family Coronaviridae, referred to as ‘2019-nCoV’.

Phylogenetic analysis of the complete viral genome (29,903 nucleotides) revealed that the virus was most closely related (89.1% nucleotide similarity) to a group of SARS-like coronaviruses (genus Betacoronavirus, subgenus Sarbecovirus) that had previously been found in bats in China. 

Although the evidence shows that SARS-CoV-2 is not a purposefully manipulated virus, it is currently impossible to prove or disprove the other theories of its origin.

SARS-CoV-2 Spreading

Based on what is currently known about this coronavirus, the CDC said on March 6, 2020, the transmission, in general, occurs much more commonly through respiratory droplets than through fomites. The spread from person-to-person happens most frequently among close contacts, living together, at home, or a nursing facility.

A study published by the JAMA on April 29, 2020, found contact investigations for SARS-CoV-2 have confirmed community transmission rates that are consistent with droplet and contact spread (household attack rates of 10%, healthcare, and community attack rates of <1%, and R0 [the effective reproduction number, or the average number of new infections caused by an infected individual during their infection] of 2-3), and much different than for airborne viral pathogens, such as measles with an R0 of 10-18.

A study published in the NEJM on April 15, 2020, suggests that the ‘volume’ of conversation matters. These NIH researchers say speaking at a normal volume could produce droplets that could carry the coronavirus and linger in the air long enough to enter the airways of others in the vicinity. And when speaking loudly, the virus transmission risk increases.

And, current evidence suggests that SARS-CoV-2 can remain viable for several hours on surfaces made from a variety of materials. Cleaning dirty surfaces followed by disinfection is the best measure to prevent respiratory illnesses in community settings.

Furthermore, a study published in NEJM on March 17, 2020, found SARS-CoV-2 remained viable in aerosols throughout the duration of the experiment (3 hours), with a reduction in infectious titer from 103.5 to 102.7 TCID50 per liter of air.

And, SARS-CoV-2 was more stable on plastic and stainless steel, than on copper and cardboard. And the coronavirus was detected up to 72 hours after application to these surfaces, although the virus titer was greatly reduced after 48 hours on stainless steel.

The SARS-CoV-2 infectious rate is estimated the R-0 as between 1.4 to 2.5, which contrasts with the seasonal influenza is a little over 1 RO.

Who Is At Higher-Risk

Early information out of China, South Korea, and Italy, shows that some people are at higher risk of getting very sick from this illness. This includes older adults and people who have serious chronic medical conditions like Heart disease, Diabetes, Lung disease.

About 35.8% of the first group of adults admitted to New York City hospitals with COVID-19 disease were diagnosed as obese, according to a research letter published in NEJM on April 17, 2020. The median age was 62.2 years, 60.6% were men.

SARS-CoV-2 Seasonality

On April 13, 2020, an analysis by scientists observed that the virus was spreading more slowly in countries with warmer climates. But, these US Homeland Security researchers said these 'results in no way suggest that SARS-CoV-2 would not spread in warm humid regions.'

On March 16, 2020, researchers at the Institute of Human Virology at the University of Maryland School of Medicine and the Global Virus Network predict that SARS-CoV-2, and COVID-19, the disease it causes, will follow a seasonal pattern similar to other respiratory viruses, such as the seasonal flu. 

A previous study published by The Lancet in 2004, discussed 'Seasonality of infectious diseases and SARS.'

SARS-CoV-2 Diversity

Like all viruses, SARS-CoV-2 evolves over time through random mutations, only some of which are caught and corrected by the virus’s error correction machinery. Over the length of its 30,000-base-pair genome, SARS-CoV-2 accumulates an average of about one to two mutations per month.

A recent paper published by Lu Jian of Peking University and colleagues on March 3, 2020, analyzed 103 virus genomes and argued that they fell into one of two distinct types, named S and L, distinguished by two mutations. Because 70% of sequenced SARS-CoV-2 genomes belong to L, the newer type, the authors concluded that the virus has evolved.

According to the CDC on March 3, 2020, scientists reported that the rate of symptomatic infection among a patient’s household members was 10.5%. And, the rate among other close contacts was found to be far less, at 0.45%.

And, a non-peer-reviewed study developed an analysis to facilitate real-time mutation tracking of the SARS-CoV-2 coronavirus, focusing initially on the Spike (S) protein because it mediates infection of human cells and is the target of most vaccine strategies and antibody-based therapeutics. As of April 30, 2020, these researchers had identified 14 mutations in the Spike.

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