The studies below are geared to the scientific community, but I provide links to these studies for those who would like more details about the intricate mechanisms and the sophisticated study designs that so quickly advanced knowledge about the pandemic virus.

Two relevant finding from these studies are of interest for the pubic. First, identifying compounds that interfere with binding of the virus (e.g., antibodies from a recovered person) is a promising strategy for designing vaccines and therapeutics to prevent future pandemics. Second, the human receptor that tightly binds virus is more highly expressed deep in the lungs (tiny air sacs or alveoli, bronchi, alveolar immune cells) than in the upper respiratory tract. It is unclear if SARS-CoV-2 infects and replicates in host cells of the upper respiratory system, but it certainly does in the deep lung tissues where the damage occurs that could lead to fatal respiratory failure. So, just presence of the virus in the nose only ensures that you’ve been exposed, not that the virus has infected your lungs.

A great desktop resource for a medical microbiologist, Schaechter’s Mechanisms of Microbial Disease, provides additional information about biological protections that limit viral spread in health humans. First, the specialized hairs in the nose (vibrissae) filter and trap particles including viruses from entering the deep lung. Next, cells lining the respiratory tract from the nose to the bronchioles in the deep lung are covered with mucous and cilia that eliminate inhaled microbes, pushing particles up the ‘escalator’ and out of the lungs (technical term, mucocilliary escalator). Anatomical characteristics of the respiratory tract also limit entry of inhaled microbes, but will not be discussed in detail here. For viruses that may make it to the deep lung alveoli, immune defenses await: antibodies, complement, alveolar macrophages that signal other immune cells to assist in removing and killing invading viruses (and bacteria). These immune defenses are also present in the mouth to process any pathogen moved up the mucocilliary escalator from the deep lung.

More recent studies (Voelker and Numata, 2019; Zhao et al., 2019; Lu et al., 2020; Varricchio et al., 2020) document in more detail the mechanisms by which our innate immune systems call on the cellular defenses mentioned above through activity of Toll-like receptors, interferon-induced transmembrane proteins, and phosopholipid to eliminate pathogens including viruses from the respiratory system.

Further, this breaking report (Thevarajan et al., 2020) documented that innate and adaptive immunity was key in recovery of a case exposed in Wuhan who traveled to Australia before illness developed. These cell types and antibodies directed against SARS-CoV-2 were detected in the blood prior to and during recovery for at least 13 days following exposure.

antibody-secreting cells (ASCs)

specific T-lymphocytes (activated CD4+ T cells; CD8+ T cells; follicular helper T cells)

immunoglobulin M (IgM) and IgG antibodies

The patient was discharged after one week of care. Changes over time (kinetics) of the sustained immune response were documented, particularly progressive increases in antibody response (both IgM and IgG) until day 20. Minimal pro-inflammatory cytokines and chemokines were detected, even during symptomatic periods at days 7-9. The authors hypothesize that understanding early adaptive immune responses might correlate with better clinical outcomes and, in the future, enhance recovery rates for severe cases of COVID-19.

Another very recent study (Guo et al., 2020) reported dramatic differences between case severity and blood chemistry and immune responses. Mild cases had normal or slightly decreased counts of white blood cells and platelets (lymphocytopenia). Severe cases had significantly higher counts of key blood components (neutrophils, D-dimer, blood urea, creatinine, interleukins IL-6 and -10, and tumor necrosis factor alpha (TNF)) and lower lymphocyte counts. In addition, ICU patients had more extreme changes in blood (higher IL-2, -7, and -10, granulocyte stimulating factor, interferon gamma induced protein, monocyte chemo-attractant proteins, macrophage inflammatory protein, and TNF) indicative of cytokine storm, septic shock, and metabolic and coagulation disorders.

MICROBIOME EFFECTS

If you know me as a scientist, you know how fascinated I am by the communities of microbes that live in and on us as partners in health: our microbiota.

You may not know that our upper and lower respiratory tracts are NOT STERILE, but have dense and diverse microbes colonizing surfaces. I encourage you to take a look at the abstracts and figures in these studies:

I am pleased to connect you with Professor Glenn Gibson, Food Microbial Sciences Unit, University of Reading, UK, through his blog Can Probiotics and Prebiotics go Viral?. In the blog, Prof. Gibson cites this double blind, randomized human clinical trial (deVrese et al., 2005) that concluded that ingestion of a specific probiotic product for 3 months shortened common cold episodes by nearly 2 days and reduced the severity of symptoms.

Prof. Gibson’s blog next mentions a more recent systematic review of multiple studies (Hao et al., 2015; Probiotics for Preventing Acute Upper Respiratory Tract Infections) that concluded ‘Probiotics were found to be better than placebo in reducing the number of participants experiencing episodes of acute [upper respiratory tract infections] URTI by about 47% and the duration of an episode of acute URTI by about 1.89 days.’

Also relevant to this conversation are a tremendous number of recent studies that document connections between the gut microbiota and dietary choices on risks of respiratory tract diseases. I highlight these studies below but invite you to contact me for more information.

BOTTOM LINE

I repeat, fear not. Social distancing and quarantine are well documented to reduce the likelihood of both exposure and illness, particularly severe illness. Even if your nasal swab tests positive for the pandemic virus SARS-CoV-2, early detection and proper care are likely to bring you to full recovery without complications involving severe pulmonary distress. WHO (2020), Figure 6A below illustrates the ‘worst-case’ scenario to date where delayed social distancing and quarantine caused high case numbers (nearly 3,000 per day for about a week at the peak in the second phase of the outbreak) that overwhelmed local resources and contributed to high local fatality rates early in the outbreak expanding from Wuhan.