Starting as a mysterious pneumonia in Wuhan, China, the newly named COVID-19 has resulted in a worldwide outbreak, causing morbidity and mortality as well as potentially disrupting the global economy. The World Health Organization (WHO) has declared this a global pandemic; to date (as this article goes to press), there are more than 80,000 reported cases worldwide (72,506 from Mainland China, Hong Kong, and Macau), and COVID-19 has claimed more than 2700 lives. (For more information, please see https://www.cdc.gov/coronavirus/ 2019-ncov/summary.html.)
Although pharmaceutical companies and countries are looking into vaccinations and curative treatment for coronavirus infection, currently there is nothing available; thus, precautions against transmission and early supportive treatment is key. Psychiatrists must have a basic understanding of the pathophysiology of coronaviruses in order to be able to accurately explain and discuss those issues with their patients, especially as mental health ramifications are expected.
Exploring the coronavirus: what is it?
Coronaviruses, belonging to the Coronaviridae family, are single‐stranded positive‐sense ribonucleic acid (RNA) viruses that thrive in animals, which are their natural carriers. The only coronaviruses previously known to infect humans were HCoV‐229E, HCoV‐OC43, HCoV‐NL63, andHKU1, as well as the two infamous relatives of 2019-nCoV—the severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS), responsible for outbreaks in 2002-2003 and 2012, respectively. Alphacoronaviruses and betacoronaviruses infect mammals (eg, bats) whereas gammacoronaviruses and deltacoronaviruses are more prone to cause fish and bird infections (Table). Animal to human—zoonotic—transmission is not the norm for coronaviruses, but prior coronavirus outbreaks in animals have been economically damaging.
It is unclear why more zoonotic epidemics have been occurring of late. However, it is hypothesized that global climate factors may be related and similar to viral mutations linked to pandemic capacity (ie, genetic drifts in a wide outbreak in animals may essentially lead to better virus survival rates in humans).1,2
In the case of COVID-19, the transmission is suspected to have occurred at the Wuhan Huanan Seafood Wholesale Market, although the exact carrier species has not been determined.3 From this point, the main 2019-nCoV contagion has been human-to-human transmission. Symptoms have ranged from mild to severe, with most patients reporting fever, dry cough, myalgia, fatigue, and diarrhea.4 Gastrointestinal symptoms have been present, although less frequent than with SARS.5
Variations in innate immune response
Why do some people get sicker than others? Coronaviruses have an RNA genome, similar to the influenza virus (responsible for the flu) or the respiratory syncytial virus (RSV). The immune system recognizes the RNA as foreign and triggers the immune response responsible for fighting the virus (ie, production of interferons and pro-inflammatory cytokines), and then clearing the foreign entity out of the body. A review of the exact immune responses are beyond the scope of this manuscript. However, the reader is encouraged to remember that the immune system is highly adaptable and modifies its metabolism and existing balance to fight expected threats (for an excellent review, see Kikkert6). Unfortunately, the virus exploits the host’s immune system, mimicking certain innate components to hide while replicating, which makes the immune system less able to effectively fight the invasion. Viruses may also halt cellular replication and use existing cellular resources to prioritize viral replication. The balance between immune response and viral replicative success ultimately determines disease outcome.
Certain populations are known to be vulnerable to COVID-19, such as infants, the elderly, and those with immunocompromised systems or pre-existing medical issues, who are at increased risk for severe repercussions from infections and, thus, more likely to develop sepsis and possibly death; worse outcomes could also be related to an overactive immune response.7 Cytokine storm, a term referring to over-production of inflammatory cytokines, was found more often in patients suffering from COVID-19 who ended up in intensive care, but causal factors are not fully understood.8 Thus far, there is no way to predict who will have an exaggerated immune response besides looking for the previously noted clinical, non-specific factors.
Dr Moukaddam is Associate Professor, Menninger Department of Psychiatry and Behavioral Science, Baylor College of Medicine, Ben Taub Adult Outpatient Services Director, Medical Director, STAR (Stabilization, Treatment, and Rehabilitation) Program for Psychosis, Houston, TX. Dr Shah is Professor & Executive Vice Chair, Barbara & Corbin J. Robertson Jr. Chair in Psychiatry at Menninger, Chief of the Division of Community Psychiatry at Baylor College of Medicine. They report no conflicts of interest concerning the subject matter of this article.
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