Background Achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and induces the disease in a genetically susceptible host. The association between achalasia and coronaviruses has not been reported. Aims To evaluate the presence of the SARS‐CoV‐2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter muscle (LESm) of achalasia patients who posteriorly had SARS‐CoV‐2 (achalasia‐COVID‐19) infection before laparoscopic Heller myotomy (LHM) and compare the findings with type II achalasia patients and transplant donors (controls) without COVID‐19. Methods The LESm of 7 achalasia‐COVID‐19 patients (diagnosed by PCR), ten achalasia patients, and ten controls without COVID‐19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and effector CD4 T cell and regulatory subsets were determined by immunohistochemistry. Key Results Coronavirus was detected in 6/7 patients‐COVID‐19. The SARS‐CoV‐2 was undetectable in the LESm of the achalasia patients and controls. ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post‐COVID‐19. The percentage of Th22/Th17/Th1/pDCreg was higher in achalasia and achalasia‐COVID‐19 pre‐HLM vs. controls. The Th2/Treg/Breg cell percentages were higher only in achalasia vs. controls. Conclusion & Inferences SARS‐CoV2 and its receptor expression in the LESm of achalasia patients who posteriorly had COVID‐19 but not in the controls suggests that it could affect the myenteric plexus. Unlike achalasia, patients‐COVID‐19 have an imbalance between effector CD4 T cells and the regulatory mechanisms. SARS‐CoV‐2 and its receptor are expressed in the lower esophageal sphincter of achalasia patients who posteriorly had COVID‐19. It suggests that SARS‐CoV‐2 could be a trigger agent for the development of achalasia through the imbalance between effector CD4 T cells and the regulatory mechanisms.