The novel coronavirus known as SARS-CoV-2 and the associated disease process COVID-19
(coronavirus disease 2019) was first seen in late 2019 in Wuhan, China. Over the following
months, it quickly spread across the continent and, in short order, the globe, making an
impact that hasn't been seen in generations. Although coronaviruses have been prevalent for
millennia, this version is immunologically novel, and thus there is no natural immunity to
the virus. This has been a major reason for its rapid spread across the world.

Previous members of the coronavirus family have typically caused upper respiratory symptoms
such as the common cold, though there have also been more virulent versions of this virus
seen in the recent past, such as SARS (Severe Acute Respiratory Syndrome) and MERS (Middle
East Respiratory Syndrome). Similarly named, SARS-CoV-2 also causes upper respiratory
symptoms but has varied from the previous viral syndromes in a number of ways including how
quickly it has been able to transmit within a population. This is a disease that does not
segregate and can affect all ages, genders, and ethnicities. Everyone is susceptible to this
virus.

New diagnostic and therapeutic approaches for respiratory viruses are also being rapidly
developed and polymerase chain reaction-based (PCR) diagnostics and multiplex assays are
increasingly used in clinical laboratories for SARS-CoV-2 clinical detection and subtyping.
Rapid antigenic and genetic evolution has been expected for SARS-CoV-2 strains, and a better
understanding of SARS-CoV-2 evolutionary dynamics is needed to establish an effective
vaccine.

Our present understanding of the nature and extent of the upper respiratory track (URT)
microbiome in humans is limited. Furthermore, we have little understanding of how acute viral
respiratory infections of SARS-CoV-2 influence the URT microbiome, or how genotypic
differences in the virus influence the URT microbiome and vice versa. Innate immune responses
to pathogens, along with dysregulation of inflammation, are key factors involved in
pathogenesis, and different viral pathogens activate different types of inflammatory
responses. Respiratory viral infection i.e., SARS-CoV-2 infection is expected to activate
TLR2, TLR3, TLR4 and TLR7 responses and this is likely to modulate commensal microbiota
populations. It is not yet known if the severity of SARS-CoV-2 disease in older adults is due
to a biased host response, SARS-CoV-2 virulence determinants, or the impact infection has on
commensal microbiota.

Up to this point, there is no unanimously approved treatment for the disease nor is there a
vaccine or antiviral drugs available for the public. The primary methods for treatment of
this deadly virus have been supportive in nature including intubation in severe cases with
respiratory failure.

While a unanimous treatment has yet to be discovered, there has been a great amount of
knowledge garnered over the last few months about the virus and the disease that accompanies
it. Several studies have demonstrated high viral titers within the nasopharynx and oral
cavity and many have posited that this is the primary source of infection and viral
replication. Additionally, a high nasal/nasopharyngeal viral load has been associated with
increased symptoms and higher severity of the disease.

Interestingly, there have been a number of studies recently looking at the effect of nasal
saline irrigations in the setting of viral URIs, including coronaviruses (not including
SARS-CoV-2). One of the major takeaways from these studies was decreased viral shedding in
patients treated with saline irrigations compared to the control group. Nasal saline
irrigations are available over the counter and widely viewed as both safe and affordable.
Could these irrigations have a similar effect on the novel SARS-CoV-2 that they have on other
viral respiratory infections?