Letter: Covid-19, and vitamin D

Biomedical Journal, 2021

Q1 COVID-19 is a recent pandemic that is still a major health problem of modern times and already more than 17.5 lakhs people succumbed to this deadly disease. This disease is caused by novel coronavirus which is named SARS-COV-2 by the International Committee on Taxonomy of Viruses. This virus originated from Wuhan city in Hubei province of China in December 2019 and within a short period spread across the many countries in the globe. There are a lot of basic as well as clinical research is going on to study the mode of transmission and the mechanism of action of SARS-COV-2 infection and its therapeutics. SARS-COV-2 is not only known to infect lungs, but it also infects other organs in the human body including the gastrointestinal (GI) tract, the liver, and the pancreas via the angiotensin-converting enzyme (ACE) 2, an important component of the renin-angiotensin system. In this short review, we are mainly discussing the mode of SARS-COV-2 transmission, physiological counterbalancing roles of ACE2 and ACE and the tissue patterns of ACE2 expression, and the overall effect of COVID19 on human gastrointestinal System. Therefore, this review sheds light on the possible mechanism of SARS-COV-2 infection in the GI system and its pathological symptoms raising a potential possibility of GI tract acting as a secondary site for SARS-CoV-2 tropism and infection. Finally, future studies to understand the fecal-oral transmission of the virus and the correlation of viral load and severity of GI symptoms are proposed to gain knowledge of the GI symptoms in COVID-19 to aid in early diagnosis and prognosis. The novel coronavirus (nCov) identified in 2019 belongs to a strain of human coronaviruses (CoVs) which include 229E, NL63, OC43, HKU1, Middle East respiratory syndrome (MERS-CoV), severe acute respiratory syndrome (SARS-CoV) [1]. Coronaviruses belong to the family Coronaviradae and further subdivided into alpha, beta, gamma, and delta genera

The Journal of Nutrition

The biomedical community is racing to better understand the mechanism of action behind the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that is causing the coronavirus disease 2019 (COVID-19) pandemic. Having a better understanding of the mechanism and characteristics that make some individuals more susceptible than others to severe symptoms and preventing viral reactivation in people who have had a history of exposure to SARS-CoV-2 will help protect everyone. We postulate here that vitamin D status may be involved in the severity of the immune response to SARS-CoV-2 infection. It is evident that the renin-angiotensin system (RAS) is involved in COVID-19 pathogenesis (1). Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II, a protein that mediates blood pressure and promotes inflammation, fibrosis, and oxidant responses through interaction with angiotensin II type I receptor (AT1) (2) (Figure 1). ACE2 converts angiotensin II to angiotensin-(1,7), and the interaction of angiotensin-(1,7) with the Mas receptor counter-regulates the inflammatory effects of angiotensin II (3). Membrane-bound ACE2 was identified as a receptor for SARS-CoV-1, the virus responsible for the 2003 SARS pandemic (4), and ACE2 is also the receptor for SARS-CoV-2 (1). SARS-CoV-2 penetrates epithelial cells by binding its transmembrane spike glycoprotein to membrane-bound ACE2. ACE2 receptors are found in lung (alveolar), heart, kidney, endothelium, and intestine (5), and ACE2 plays an important role in counterbalancing the negative proinflammatory downstream effects triggered by angiotensin II binding to AT1. Although SARS-CoV-2 must bind with ACE2 to penetrate cells, it also simultaneously downregulates ACE2, subsequently causing the receptors to lose function (6). ACE2 is critical for protecting against tissue damage, so loss of function of ACE2 can promote acute lung damage caused by angiotensin II (4, 7). Preliminary data show that the mortality rate from COVID-19 is lower in countries proximal to the equator compared with more distal countries (8). A higher rate of infection and

Frontiers in Pediatrics, 2021

Coronavirus disease 2019 (COVID-19), caused by acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is predominantly a respiratory disease. However, its significant impact on the gastrointestinal (GI) system is now well-known. SARS-CoV-2 enters cells via the angiotensin-converting enzyme-2 (ACE-2) receptor, which is abundantly expressed on lung cells, but also on enterocytes. Several etiopathogenetic mechanisms have been postulated to explain the GI involvement in COVID-19, including loss in intestinal absorption, microscopic mucosal inflammation and impaired ACE-2 function, which plays a significant role in maintaining gut homeostasis. In children the GI manifestations include anorexia, nausea, vomiting, diarrhea and abdominal pain, which may represent the earliest presenting symptoms of the disease. However, although rare, a significant GI mucosal inflammation, such as terminal ileitis mimicking an atypical appendicitis, and other GI manifestations have been reported. COVID-19 p...

Journal of Community Hospital Internal Medicine Perspectives

SARS-CoV2 is a novel coronavirus responsible for causing COVID-19, first identified in the city of Wuhan, China and officially declared a pandemic by the World Health Organization. SARS-CoV2 expresses high affinity to human ACE2 receptors, including within the gastrointestinal tract. Patients with COVID-19 exhibit a wide spectrum of GI symptoms including anorexia, nausea, vomiting, abdominal pain, and abnormal liver function tests. Pathogenesis behind gastrointestinal symptoms caused by SARS-CoV2 has been postulated to be multifactorial including disruption of the intestinal mechanical barrier integrity, alteration of the gut microbiome and systemic inflammatory response to the virus. SARS-CoV-2 RNA has also been found in stool samples of infected patients for a significantly longer period than in nasopharyngeal samples, though the implication of this finding is unclear at this time. Liver injury in patients with COVID-19 is usually mild, stemming from immune-mediated damage, drug induced hepatotoxicity, or ischemia from sepsis. Patients with pre-existing liver disease may be at a higher risk for hospitalization and mortality. Given the high degree of infectivity of this disease, healthcare providers will need to remain watchful for resurgence of this virus. Strict protocols should be implemented regarding hand hygiene, isolation, personal protective equipment, and appropriate disposal of waste. It is also imperative to identify patients with gastrointestinal symptoms at an early stage as these patients may have a prolonged course between symptom onset and viral clearance.

2020

Since December 2019 a global epidemic of the novel coronavirus disease (Covid19) started, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Unfolding the natural history of the disease proved that although the predominant site of infection is the lungs, about one third of Covid19 patients present extrapulmonary symptoms especially in the gastrointestinal (GI) system such as anorexia, diarrhea, vomiting, and abdominal pain. SARS-CoV-2 can actively infect and replicate in the GI tract through its entry receptor angiotensin converting enzyme 2 (ACE2) that is highly expressed in both alveolar and GI epithelial cells. These findings imply the possible involvement of the gut microbiota, which is known to influence the effectiveness of lung immunity. The aim of this rapid-review is to provide an update of the impact of Covid19 infection on the GI tract with a special focus on the microbiome. A better understanding of the relationship between Covid19 and the digest...

International Journal of Celiac Disease, 2020

The severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) dwells in the respiratory airways, however, its digestive tract presence, infectivity, mucosal attachment and penetrating mechanisms, enteric proliferation, stool shading, flashed bio-aerosol spreading and fecal-oral transmission is far from being understood. The present review opens some skylights to lighten the long, tortuous, dark and challenging tunnel of the gastrointestinal tract and his uninvited covid-19 viral new inhabitant.

Med Hypotheses, 2020

The pandemic of acute respiratory illness caused by the novel betacoronavirus SARS-CoV-2, officially designated COVID-19, has attained the proportions of a global health crisis. Though all nations of the world have been affected by this disease, there have been marked cross-national variations in prevalence, severity and mortality rates. Various explanations, based on demographic, social and climatic factors, have been suggested to account for this variability, but these remain unverified to date. Based on recent research findings suggesting that human enterocytes may serve as a point of entry for SARS-CoV-2, leading to intestinal viral replication, this paper puts forward the hypothesis that prior intestinal infection with coronaviruses, either symptomatic or asymptomatic, may moderate this process and minimize the severity of SARS-CoV-2 infection. This hypothesis is supported by evidence on the gastrointestinal manifestations of SARS-CoV-2 and related infections, on the geographic...

Journal of Digestive Diseases, 2020

Archives of Physiology and Biochemistry

In December 2019, a new infectious complication called CoronaVirus Infectious Disease-19, briefly COVID-19, caused by SARS-COV-2, is identified in Wuhan, China. It spread all over the world and became a pandemic. In many individuals who had suffered SARS-COV-2 infection, cytokine storm starts through cytokine overproduction and leads to Acute Respiratory Syndrome (ARS), organ failure, and death. According to the obtained evidence, Vitamin D (VitD) enhances the ACE2/Ang(1-7)/MasR pathway activity, and it also reduces cytokine storms and the ARS risk. Therefore, VitD intake may be beneficial for patients with SARS-COV-2 infection exposed to cytokine storm but do not suffer hypotension. In the present review, we have explained the effects of VitD on the renin-angiotensin system (RAS) function and angiotensin-converting enzyme2 (ACE2) expression. Furthermore, we have reviewed the biochemical and immunological effects of VitD on immune function in the underlying diseases and its role in the COVID-19 pandemic.

BJSTR, 2021