# Inflammation Causes Exacerbation of COVID-19: How about Skin Inflammation?
###### Abstract  
COVID-19 is a recently emerged viral infection worldwide. SARS-CoV-2, the causative virus, is believed to have emerged from bat coronavirus, probably through host conversion. The bat coronavirus which has the highest gene homology to SARS-CoV-2 specifically infects deep forest bats in China whose habitat extends through the Middle East to Southern Europe. Host conversion might have occurred due to the deforestation by humans exposing wild bats to the environment they had never encountered before. SARS-CoV-2 infects cells through two mechanisms: through its receptor ACE2 with the help of enzyme TMPRSS and through membrane fusion with the help of elastases in the inflammatory condition. Obesity, hypertension, diabetes mellitus, and pulmonary diseases cause poor prognosis of COVID-19. Aging is another factor promoting poor prognosis. These diseases and aging cause low-level and persistent inflammation in humans, which can promote poor prognosis of COVID-19. Psoriasis and atopic dermatitis are the major inflammatory skin diseases. These inflammatory skin conditions, however, do not seem to cause poor prognosis for COVID-19 based on the epidemiological data accumulated so far. These mechanisms need to be elucidated. t pacs: atopic dermatitis; COVID-19; inflammation; psoriasis; skin; SARS-CoV-2 +
Footnote †: journal: Medical Sciences  
reports demonstrate evidence implying its existence earlier than widely believed [2]. SARS-CoV-2 is the seventh member of the coronavirus family to infect humans. The common cold is usually caused by four varieties of coronaviruses (HCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1) which evoke a wide range of upper respiratory infection symptoms. MARS-COV and SARS-CoV are responsible for severe atypical pneumonia and utilize dipeptidyl peptidase 4 (DPP4) and angiotensin-converting enzyme 2 (ACE2), respectively, as their receptors to enter human cells distributed abundantly in the lower respiratory tract in humans [3]. The SARS-CoV-2 genome sequence shares 70% similarity with SARS-CoV and utilizes the same receptor as SARS-CoV, but with a 10-to-20-fold higher affinity, which makes human-to-human transmission easier [4]. The origin of SARS-CoV-2 is still uncertain, but it is believed that it originated from bat coronaviruses. Bats with thousands of gene types live deep in the mountains and forests of China, and various subspecies of coronaviruses infect specific genetic types of bats. The specificity has been strictly conserved; however, the specificity loosens when the environment changes, such as in case of the virus-bat relationship, resulting in host conversion [5; 6; 7]. The genetic state is very unstable when host conversion occurs, which might have allowed coronaviruses to infect humans when otherwise they had not. Among them, RatG13 is the coronavirus subspecies with the highest genetic homology with SARS-CoV-2 [2]. This virus specifically infects greater horseshoe bats (_Rhinolophus ferumequinum_) which live in wide areas in China and are dispersed throughout the Middle East to Southern Europe. The coronavirus detected in this species of bats in the deep forests of China is genetically very similar to SARS-CoV-2 with an overall 96.2% genome sequence identity. The S gene, which encodes the receptor binding the spike protein of the coronavirus, is highly divergent between various coronaviruses. The other SARS-related coronaviruses showed a less than 75% sequence identity, while RatG13 showed an almost 93% identity with the SARS-CoV-2 S gene sequence [2]. There might have been an intermediate host which mediated the SARS-CoV-2 infection from bat to humans. In SARS-CoV, the palm civet is one possible intermediate host, and for MARS, the dromedary is thought to be the mediator. In SARS-CoV-2, the pangolin is thought to be the possible intermediate host [6]. Pangolins are the most poached mammals in the world according to the World Wide Fund for Nature (WWF) (Pangolin! Species! WWF, worldwildlife.org, accessed on 9 September 2022).