Cough is considered as one of the most common symptoms related to an acute viral upper respiratory tract infection (URI). Acute cough is defined as cough of less than 3 weeks’ duration, and is transient and self-limited. On the contrary, few individuals recovering from a common cold syndrome, can show persistent symptoms of dry, troublesome cough. Though standard accepted terminology includes subacute cough as a cough lasting 3–8 weeks, whereas chronic cough persisting for greater than 8 weeks.

Numerous hypothesis suggest different mechanisms to clarify viral URI-induced cough along with prolonged cough reflex hypersensitivity after acute URI. Trials evaluating cough reflex sensitivity with the help of a capsaicin cough challenge, have shown that the sensitivity of the cough reflex can increase during acute viral URI and can continue so for a month or more even after resolution of the viral syndrome.

The emergence of COVID-19 pandemic has raised concerns whether infection with SARS-CoV-2 would cause a prolonged postviral cough, such as traditionally been seen after other acute viral respiratory tract infections each year. Initial studies appraising the post-COVID-19 patients did not reveal high incidence of post-COVID-19 chronic cough and, in cases where such a persistent cough occurred, it appeared as non-severe and did not negatively affected the patient.

Several studies also showed the higher prevalence of symptoms other than cough (like fatigue, dyspnea with exertion and chest tightness/discomfort) in patients after SARS-CoV-2 infection. One of such study that included 143 patients who had been hospitalized for COVID-19 and subsequently discharged, at a mean of 60.3 days after symptom onset showed fatigue, dyspnea, joint pain and chest pain as more commonly encountered symptoms than cough. Similar findings were corroborated with another study that demonstrated that included 110 patients who had been hospitalized with COVID-19 and were analysed at a median (IQR) of 90 (80–97) days after symptom onset. The investigators showed fatigue and breathlessness as more common symptoms, which were seen in39% of the cohort as residual symptoms, whereas cough was seen in only 11.6% patients.

Various viable hypotheses support the appearance of coughing during active SARS-CoV-2 infection as the primary site of entrance for COVID-19 is the respiratory epithelium. The vagal sensory nerves that play an important role in modulating cough terminate in the epithelium and subepithelial mucosa of the human airways. Airway epithelial cells produce and release many autacoids, growth factors and cytokines that can engage receptors and ion channels on the peripheral terminals of airway sensory nerves to trigger action potential discharge and coughing. SARS-CoV-2 utilizes the cell surface protein angiotensin-converting enzyme type 2 (ACE2) for docking and cellular entry on mucosal surfaces. ACE2 is expressed in upper and lower airway epithelial cells and regulates mucosal concentrations of the pro-inflammatory peptide bradykinin which is responsible for the severe systemic consequences of SARS-CoV-2 infection. Additionally, bradykinin is also known to stimulate coughing. Thus, occurrence of cough during infection could be the outcome of an epithelial cell insult resulting in the release of pro-inflammatory autacoids, neurotrophins, cytokines and alarmins, which can trigger coughing or sensitize the airways to mucosal irritation.

Therefore, it can be concluded that postviral chronic cough is uncommon and can not be regarded as debilitating residual effect. Plethora of evidence suggest that symptoms of fatigue, dyspnea and chest tightness/discomfort have higher prevalence Covid-19 patients in contrast to cough.

Source: Dicpinigaitis PV, Canning BJ. Is There (Will There Be) a Post-COVID-19 Chronic Cough? Lung. 2020 Dec;198(6):863-865.