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.