{"title":"Aflatoxin B1 and viruses’ combined pathogenesis: A mini systematics review of invitro and invivo studies","authors":"Mehdi Ahmadi , Ramin Shahbahrami , Fatemeh Khajeh , Sepideh Khodaeivandi , Ehsan Kakavandi , Reza Hazrati Raziabad , Kiandokht Ghanati","doi":"10.1016/j.acthis.2023.152116","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><p><span><span>The combined pathogenesis of Aflatoxin B1<span> (AFB1) and several viruses such as </span></span>HBV, </span>EBV and influenza virus have been investigated yet the molecular mechanism of their interaction and possible synergistic effects is not fully understood.</p></div><div><h3>Objectives</h3><p>The aim of the current systematic review<span> was to review in-vitro and in-vivo studies investigating the combined pathogenesis of aflatoxins and viruses.</span></p></div><div><h3>Methods</h3><p>This systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. PECO (Population, Exposure, Comparator, and Outcome) criteria for invitro and invivo studies were used to evaluate the eligibility of the studies for systematic review.</p></div><div><h3>Results</h3><p>21 studies were eligible for qualitative analysis based on the inclusion criteria. Of all the included studies, 9 (42.9 %) were invivo, 7 (33.3 %) were invitro-invivo and 5(23.8) articles conducted only invitro assay. Furthermore 14 (66.6 %) article explored hepatitis B virus (HBV) combination with AFB1, 4 (19 %) studied influenza A virus (SIV), 2 (9.7 %) were about Epstein–Barr virus (EBV) and only 1 (4.7 %) included hepatitis C virus (HCV).</p></div><div><h3>Conclusion</h3><p>The limited collected evidence suggests that AFB1 enhanced EBV and influenza virus pathogenesis. AFB1 also operated as a cofactor for HBV and EBV-mediated carcinogenesis. On the other hand HBV and HCV also induced AFB-1 carcinogenesis. Due to the limited amount of included studies and the inconsistency of their results further studies especially on HBV and SIV are essential for better understanding of their combined mechanisms.</p></div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S006512812300123X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction
The combined pathogenesis of Aflatoxin B1 (AFB1) and several viruses such as HBV, EBV and influenza virus have been investigated yet the molecular mechanism of their interaction and possible synergistic effects is not fully understood.
Objectives
The aim of the current systematic review was to review in-vitro and in-vivo studies investigating the combined pathogenesis of aflatoxins and viruses.
Methods
This systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. PECO (Population, Exposure, Comparator, and Outcome) criteria for invitro and invivo studies were used to evaluate the eligibility of the studies for systematic review.
Results
21 studies were eligible for qualitative analysis based on the inclusion criteria. Of all the included studies, 9 (42.9 %) were invivo, 7 (33.3 %) were invitro-invivo and 5(23.8) articles conducted only invitro assay. Furthermore 14 (66.6 %) article explored hepatitis B virus (HBV) combination with AFB1, 4 (19 %) studied influenza A virus (SIV), 2 (9.7 %) were about Epstein–Barr virus (EBV) and only 1 (4.7 %) included hepatitis C virus (HCV).
Conclusion
The limited collected evidence suggests that AFB1 enhanced EBV and influenza virus pathogenesis. AFB1 also operated as a cofactor for HBV and EBV-mediated carcinogenesis. On the other hand HBV and HCV also induced AFB-1 carcinogenesis. Due to the limited amount of included studies and the inconsistency of their results further studies especially on HBV and SIV are essential for better understanding of their combined mechanisms.