The COVID-19 Pandemic and Post-Infection Irritable Bowel Syndrome: What Lies Ahead for Gastroenterologists

Non-ulcer Dyspepsia and Duodenal Eosinophilia: An Adult Endoscopic Population-Based Case-Control Study

Redux: Do Little Bellyachers Grow up to Become Big Bellyachers?

Potential Long Coronavirus Disease 2019 Gastrointestinal Symptoms 6 Months After Coronavirus Infection Are Associated With Mental Health Symptoms

Rear Window—What Can the Gut Tell Us About Long-COVID?

The Narcotic Bowel Syndrome: Clinical Features, Pathophysiology, and Management

Manipulation of the Microbiota for Treatment of IBS and IBD—Challenges and Controversies

Targeting the Gut Microbiota in Coronavirus Disease 2019: Hype or Hope?

AGA Rapid Recommendations for Gastrointestinal Procedures During the COVID-19 Pandemic

COVID-19 in Kidney Transplantation: Outcomes, Immunosuppression Management, and Operational Challenges.

Dyspepsia and Irritable Bowel Syndrome After a Salmonella Gastroenteritis Outbreak: One-Year Follow-up Cohort Study

Functional Bowel Disorders

Development of Abdominal Pain and IBS Following Gynecological Surgery: A Prospective, Controlled Study

SARS-CoV-2 Infection in the Gastrointestinal Tract: Fecal–Oral Route of Transmission for COVID-19?

Functional Abdominal Pain Syndrome

Viruses require specific cellular receptors to infect their target cells. Angiotensin-converting enzyme 2 (ACE2) is a cellular receptor for two divergent coronaviruses, SARS coronavirus (SARS-CoV) and human coronavirus NL63 (HCoV-NL63). In addition to hostcell receptors, lysosomal cysteine proteases are required for productive infection by some viruses. Here we show that SARS-CoV, but not HCoV-NL63, utilizes the enzymatic activity of the cysteine protease cathepsin L to infect ACE2-expressing cells. Inhibitors of cathepsin L blocked infection by SARS-CoV and by a retrovirus pseudotyped with the SARS-CoV spike (S) protein but not infection by HCoV-NL63 or a retrovirus pseudotyped with the HCoV-NL63 S protein. Expression of exogenous cathepsin L substantially enhanced infection mediated by the SARS-CoV S protein and by filovirus GP proteins but not by the HCoV-NL63 S protein or the vesicular stomatitis virus G protein. Finally, an inhibitor of endosomal acidification had substantially less effect on infection mediated by the HCoV-NL63 S protein than on that mediated by the SARS-CoV S protein. Our data indicate that two coronaviruses that utilize a common receptor nonetheless enter cells through distinct mechanisms.