Journal of Neurogastroenterology and Motility : eISSN 2093-0887 / pISSN 2093-0879

Table. 2.

Viral Infection in Achalasia

Researcher Population Methods Viruses Results
Jones et al,62 1983 Achalasia (n = 18) Complement fixation test; haemagglutination inhibition test MV Serum antibody titers against MV increased 3 fold in patients with achalasia.
Control (n = 12)
Robertson et al,63 1993 Achalasia (n = 58) Complement fixation test; in situ DNA hybridisation VZV The incidence of VZV antibodies was significantly greater in achalasia.
Control (n = 40) HSV-1 VZV was detected in 3/9 achalasia.
CMV No positive results were obtained for HSV-1or CMV.
Niwamoto et al,65 1995 Achalasia (n = 12) PCR amplification;automated DNA sequence analysis HSV 92-bp fragments were identified in nearly all specimens, which were identical to a single HSV sequence.
Control (n = 116)
Birgisson et al,71 1997 Achalasia (n = 13) PCR amplification;automated DNA sequence analysis HSV-1/2, CMV, EBV, VZV, HHV-6, MV, HPV No amplified products were seen in the achalasia specimens or controls corresponding to any of the virus sequences tested.
Control (n = 15)
Castagliuolo et al,66 2004 Achalasia (n = 15) Esophageal mononuclear cell proliferation assay;ELISA HSV-1 The prevalence of circulating anti–HSV-1 and HSV-2 antibodies proved similar in the 2 groups.
Control (n = 8) After incubation with HSV-1, mononuclear cells from achalasia patients showed a 3.4-fold increase and a 1.4-fold increase in interferon-gamma release.
Facco et al,67 2008 Achalasia (n = 59) ELISA; esophageal mononuclear cell proliferation assay HSV-1 HSV-1 DNA was detected in both patients (63%) and control (68%).
Control (n = 38) Being exposed to HSV-1 increased monocyte proliferation and released IFN-γ and IL-2 in achalasia.
Villanacci et al,30 2010 Achalasia (n = 12) IHC; in situ DNA hybridisation HSV All patients were completely negative for the presence of both HSV and HPV.
Control (n = 7) HPV
Lau et al,64 2010 Achalasia (n = 151) PCR; RT-qPCR; ELISA HSV-1 There was no difference in the positive rate of serum HSV-1 between achalasia and control, but higher in saliva (7.9%).
Control (n = 118) HSV-1 stimulation increased IFN-γ expression by 61.33 times in achalasia.
Moradi et al,72 2018 Achalasia (n = 52) PCR; RT-PCR Neurotropic and non-neurotropic viruses No association between the virus and achalasia was detected.
Control (n = 50)
Kanda et al,68 2021 Achalasia (n = 11) RT-qPCR HSV-1 The expression of HSV1-miR-H1 target ATG16L1 was significantly reduced in the LES of achalasia.
Control (n = 6)
Naik et al,69 2021 Achalasia (n = 15) Nested-RCR;RT-PCR; immunocytochemistry VZV VZV DNA was detected in 80% of the saliva and VZV transcripts were detected in 87% of the LES in achalasia.
Control (n = 5) VZV late proteins (gE, gH, and ORF40p) were detected in enteric neuronal cell bodies and nerve fibers.
Gaber et al,70 2022 Achalasia (n = 6769) Correlation analysis VZV The presence of any of the autoimmune conditions and viral infections (VZV and HPV) were associated with increased odds of achalasia.
Control (n = 27 076) HPV

MV, measles virus; VZV, varicella-zoster virus; HSV-1/2, herpes simplex virus type 1/2; CMV, cytomegalovirus; PCR, polymerase chain reaction; EBV, Epstein-Barr virus; HHV-6, human herpes virus 6; HPV, papillomavirus; ELISA, enzyme linked immunosorbent assay; RT-qPCR, reverse transcription quantitative real-time PCR; IHC, immunohistochemistry; ATG16L1, autophagy-associated 16-like protein 1; LES, lower esophageal sphincter.

J Neurogastroenterol Motil 2023;29:145~155 https://doi.org/10.5056/jnm22176
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