COVID-19: faecal–oral transmission?

Hindson, Jordan

doi:10.1038/s41575-020-0295-7

Cited by 318 publications

(290 citation statements)

References 5 publications

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“…TMPRSS2 is also widely expressed in multiple tissues including those in the GI system, lung, and kidney. The high expression of CTSL and TRMPSS2 transcripts in a series of organs could explain the viral manifestation in these tissues such as recent studies showing viral presence in stool samples from infected individuals 19 as well as effects of the virus seen across tissues. This is assuming that there is enough ACE2 expression on the tissue for viral S protein to bind and target the cell.…”

Section: Drug Screenmentioning

confidence: 99%

“Amantadine disrupts lysosomal gene expression; potential therapy for COVID19”

Smieszek

Przychodzen

Polymeropoulos

2020

Preprint

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SARS-coronavirus 2 is the causal agent of the COVID-19 outbreak. SARS-Cov-2 entry into a cell is dependent upon binding of the viral spike (S) protein to cellular receptor and on cleavage of the spike protein by the host cell proteases such as Cathepsin L and Cathepsin B. CTSL/B are crucial elements of lysosomal pathway and both enzymes are almost exclusively located in the lysosomes.CTSL disruption offers potential for CoVID-19 therapies. The mechanisms of disruption include: decreasing expression of CTSL, direct inhibition of CTSL activity and affecting the conditions of CTSL environment (increase pH in lysosomes).We have conducted a high throughput drug screen gene expression analysis to identify compounds that would downregulate the expression of CTSL/CTSB. One of the top significant results shown to downregulate the expression of the CTSL gene is Amantadine. Amantadine was approved by the US Food and Drug Administration in 1968 as a prophylactic agent for influenza and later for Parkinson's disease. It is available as a generic drug.. Amantadine in addition to downregulating CTSL appears to further disrupt lysosomal pathway , hence interfering with the capacity of the virus to replicate. It acts as a lysosomotropic agent altering the CTSL functional environment. We hypothesize that Amantadine could decrease the viral load in SARS-CoV-2 positive patients and as such it may serve as a potent therapeutic decreasing the replication and infectivity of the virus likely leading to better clinical outcomes. Clinical studies will be needed to examine the therapeutic utility of amantadine in COVID-19 infection.was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission.

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Section: Drug Screenmentioning

confidence: 99%

“Amantadine disrupts lysosomal gene expression; potential therapy for COVID19”

Smieszek

Przychodzen

Polymeropoulos

2020

Preprint

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“…Ref. [7] Indeed, it was reported that the rectal swabs showed positive results even after the nasopharyngeal tests were constitutively negative [8]. Besides, the live virus was also detected in stool samples of diseased patients.…”

Section: General Clinical Features Of Covid-19mentioning

confidence: 99%

A Review of SARS-CoV-2 and the Ongoing Clinical Trials

Chien

Yarmishyn

et al. 2020

IJMS

633

697

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The sudden outbreak of 2019 novel coronavirus (2019-nCoV, later named SARS-CoV-2) in Wuhan, China, which rapidly grew into a global pandemic, marked the third introduction of a virulent coronavirus into the human society, affecting not only the healthcare system, but also the global economy. Although our understanding of coronaviruses has undergone a huge leap after two precedents, the effective approaches to treatment and epidemiological control are still lacking. In this article, we present a succinct overview of the epidemiology, clinical features, and molecular characteristics of SARS-CoV-2. We summarize the current epidemiological and clinical data from the initial Wuhan studies, and emphasize several features of SARS-CoV-2, which differentiate it from SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), such as high variability of disease presentation. We systematize the current clinical trials that have been rapidly initiated after the outbreak of COVID-19 pandemic. Whereas the trials on SARS-CoV-2 genome-based specific vaccines and therapeutic antibodies are currently being tested, this solution is more long-term, as they require thorough testing of their safety. On the other hand, the repurposing of the existing therapeutic agents previously designed for other virus infections and pathologies happens to be the only practical approach as a rapid response measure to the emergent pandemic, as most of these agents have already been tested for their safety. These agents can be divided into two broad categories, those that can directly target the virus replication cycle, and those based on immunotherapy approaches either aimed to boost innate antiviral immune responses or alleviate damage induced by dysregulated inflammatory responses. The initial clinical studies revealed the promising therapeutic potential of several of such drugs, including favipiravir, a broad-spectrum antiviral drug that interferes with the viral replication, and hydroxychloroquine, the repurposed antimalarial drug that interferes with the virus endosomal entry pathway. We speculate that the current pandemic emergency will be a trigger for more systematic drug repurposing design approaches based on big data analysis.

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“…As of April 3, 2020, 12 deaths (9 male) were reported among the 275 patients with IBD and COVID-19 in the international Surveillance Epidemiology of Coronavirus Under Research Exclusion (SECURE)-IBD database. Of those, three patients were younger than 65 years old, and all received treatment with more than one immunosuppressant (steroid+ JAK inhibitor; adalimumab+methotrexate; adalimumab+ azathioprine+steroid) (19). Nevertheless, these cases should be interpreted with caution since many cases with mild disease were not tested for COVID-19.…”

Section: ' Introductionmentioning

confidence: 99%