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Hepatitis A virus (HAV) is the most common food-borne hepatitis in the world. The study objectives were (i) to describe the epidemiology of HAV-related hospitalizations during 1997-2011 in Taiwan, (ii) to examine the age effect on the length of stay (LOS) in hospital and (iii) to study the factors associated with death. The hospitalized cases were...
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Background
Many developing countries are experiencing the epidemiological transition, with the majority of deaths attributed to cardiovascular disease, cancer, Type 2 diabetes (T2DM) and others. In some countries, large proportional mortality attributed to diabetes is evident in official mortality statistics, with Mauritius and Fiji rated as the hi...
Citations
... Hepatitis A virus is primarily transmitted through the fecal-oral route, including person-to-person contact. In response to the virus, the immune system can cause damage to hepatocytes [6,7]. Hepatitis A poses a significant global health threat, with nearly 200 million people infected and 30,000 deaths caused by the virus each year [8-10]. ...
... Hepatitis A is a viral infection caused by the Hepatitis A virus (HAV), a single-stranded RNA virus from the Picornaviridae family [23]. HAV is commonly transmitted through the fecal-oral route (through ingestion of contaminated food or water), person-to-person contact and men who have sex with men (MSM) [24,25] and may be responsible for forms of acute hepatitis that may progress to fulminant hepatic failure in non-immune adult populations [26,27]. ...
People living with HIV (PLWH) remain at high risk of mortality and morbidity from vaccine-preventable diseases, even though antiretroviral therapy (ART) has restored life expectancy and general well-being. When, which, and how many doses of vaccine should be administered over the lifetime of PLWH are questions that have become clinically relevant. Immune responses to most vaccines are known to be impaired in PLWH. Effective control of viremia with ART and restored CD4+ T-cell count are correlated with an improvement in responsiveness to routine vaccines. However, the presence of immune alterations, comorbidities and co-infections may alter it. In this article, we provide a comprehensive review of the literature on immune responses to different vaccines in the setting of HIV infection, emphasizing the potential effect of HIV-related factors and presence of comorbidities in modulating such responses. A better understanding of these issues will help guide vaccination and prevention strategies for PLWH.
... 14 The mortality rate in different liver-associat-ed abnormalities is summarized in Table 1. [15][16][17][18][19][20][21][22][23] NAFLD is considered the most common liver disease in developed countries and is prevalent in ∼25% of the world population. 24 The disease is characterized by hepatic lipid accumulation rather than alcohol consumption. ...
Background and objectives
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in developed countries, contributing to ∼24% of cases worldwide and includes non-alcoholic steatohepatitis. NAFLD is characterized by lipid accumulation rather than alcohol consumption. There are several diagnostic/prognostic biomarkers for NAFLD including CK-18, ALT, AST, GGT, and haptoglobin, but with limited sensitivity and specificity. Therefore, high-throughput OMICS approaches have been used to characterize NAFLD conditions for the identification of potential molecular signatures or differentially regulated molecules (DEMs) and early detection of NAFLD.
Methods
We analyzed the publically available data set (accession number: GSE63067) from the Gene Expression Omnibus (GEO) using the GEO2R program. The differentially expressed genes (DEGs) were filtered using the criteria where genes with p-value ≤0.05 and fold-change ≥2.0-fold (upregulated), and fold-change ≤0.5-fold (downregulated).
Results
We identified 264 differentially expressed genes (DEGs) between NAFLD and normal liver tissue samples, where 211 were upregulated and 53 were downregulated in NAFLD. Additionally, we identified novel genes SGMS2, and WNK3 that were not well understood in the molecular pathophysiology of NAFLD. Further gene ontology-based analysis revealed that among biological processes, cellular components, and molecular functions were also dysregulated in NAFLD. Collectively, this integration of a systemic-cum-meta-analysis approach suggests that an OMICS-based analysis may provide better solutions if microarray and other high-throughput study-based DEMs are to be cataloged systematically for sharing with the scientific community. This will allow potential candidates (DEMs) to be interrogated either alone or in combination with existing biomarkers for effective early detection and or diagnosis of NAFLD.
Conclusions
Our study shows that meta-analysis of publicly available data could be a good source for identification of DEGs in NAFLD, and it can be easily extrapolated in other disease conditions.
... This sex differential was especially pronounced among infants. In a 15-year nationwide epidemiological study in Taiwan, there were higher hospitalization rates in males while male sex and age over 40 years were significant factors associated with mortality [31]. In the study of HAV patients in Saudi Arabia, no sex differences were among hospitalized patients [12]. ...
Background:
Possible sex differences in hepatitis A virus (HAV) incidence rates in different age groups are not well documented. We aimed to obtain stable pooled estimates of such differences based on data from a number of high-income countries.
Methods:
We obtained data on incident cases of HAV by sex and age group over a period of 6-25 years from nine countries: Australia, Canada, Czech Republic, Finland, Germany, Israel, Netherland, New Zealand and Spain. Male to female incidence rate ratios (IRR) were computed for each year, by country and age group. For each age group, we used meta-analytic methods to combine the IRRs. Meta-regression was conducted to estimate the effects of age, country, and time period on the IRR.
Results:
A male excess in incidence rates was consistently observed in all age groups, although in the youngest and oldest age groups, where the numbers tended to be lower, the lower bounds of the 95% confidence intervals for the IRRs were less than one. In the age groups <1, 1-4, 5-9, 10-14, 15-44, 45-64 and 65+, the pooled IRRs (with 95% CI) over countries and time periods were 1.18 (0.94,1.48), 1.22 (1.16,1.29), 1.07 (1.03,1.11), 1.09 (1.04,1.14), 1.46 (1.30,1.64), 1.32 (1.15,1.51) and 1.10 (0.99,1.23) respectively.
Conclusions:
The excess HAV incidence rates in young males, pooled over a number of countries, suggest that the sex differences are likely to be due at least in part to physiological and biological differences and not just behavioral factors. At older ages, differential exposure plays an important role. These findings, seen in the context of the excess incidence rates in young males for many other infectious diseases, can provide further keys to the mechanisms of the infection.
... In general, HAV infections spontaneously resolve with or without any symptoms of acute hepatitis, although intensive care, including urgent liver transplantation, is required to treat patients with acute liver failure (3). Previous studies have demonstrated that age over 40 years and comorbid diseases, such as diabetes, cardiovascular diseases, chronic kidney diseases, and chronic liver diseases, are associated with death in HAV-infected patients (4)(5)(6). ...
Amantadine, a nonspecific antiviral medication, also effectively inhibits HAV replication. Autophagy is an important cellular mechanism in several virus-host cell interactions.
... However, in cases of HAV-associated acute liver failure (ALF) (0.015-0.5%), intensive care, including urgent liver transplantation, is required [2]. Reported risk factors for severe acute hepatitis or for higher mortality induced by HAV infection include an age of more than 40 years, preexisting liver disease, diabetes mellitus, and cardiovascular disease [3,4]. Adjusted odds ratios for death by age 40-59 years and age over 60 years are 7.89 and 14.88, respectively, compared to age 0-19 years [3]. ...
... Reported risk factors for severe acute hepatitis or for higher mortality induced by HAV infection include an age of more than 40 years, preexisting liver disease, diabetes mellitus, and cardiovascular disease [3,4]. Adjusted odds ratios for death by age 40-59 years and age over 60 years are 7.89 and 14.88, respectively, compared to age 0-19 years [3]. Adjusted odds ratios for death by preexisting nonviral liver disease, history of hepatitis B, diabetes, and cardiovascular disease are 5.2, 2.4, 2.2, and 2.2, respectively [4]. ...
Hepatitis A virus (HAV) is a causative agent of acute hepatitis and can occasionally induce acute liver failure. However, specific potent anti-HAV drug is not available on the market currently. Thus, we investigated several novel therapeutic drugs through a drug repositioning approach, targeting ribonucleic acid (RNA)-dependent RNA polymerase and RNA-dependent deoxyribonucleic acid polymerase. In the present study, we examined the anti-HAV activity of 18 drugs by measuring the HAV subgenomic replicon and HAV HA11-1299 genotype IIIA replication in human hepatoma cell lines, using a reporter assay and real-time reverse transcription polymerase chain reaction, respectively. Mutagenesis of the HAV 5’ untranslated region was also examined by next-generation sequencing. These specific parameters were explored because lethal mutagenesis has emerged as a novel potential therapeutic approach to treat RNA virus infections. Favipiravir inhibited HAV replication in both Huh7 and PLC/PRF/5 cells, although ribavirin inhibited HAV replication in only Huh7 cells. Next-generation sequencing demonstrated that favipiravir could introduce nucleotide mutations into the HAV genome more than ribavirin. In conclusion, favipiravir could introduce nucleotide mutations into the HAV genome and work as an antiviral against HAV infection. Provided that further in vivo experiments confirm its efficacy, favipiravir would be useful for the treatment of severe HAV infection.
... Differences in immune responses have been observed also between males and females of other mammals (17)(18)(19), birds (20), reptiles (21), echinoderms (22) and insects (23). Such baseline differences can contribute to sex biases in response to pathogens (24,25 and see the next section) and to vaccination (2)(3)(4)(5)(6). Females usually have more efficient response to vaccination than males (2)(3)(4)(5), but also develop more often adverse reactions to vaccination (4,5). ...
... Male sex was associated with higher death rate in hepatitis A virushospitalized cases (24). Male sex was also a risk factor for hepatitis B virus (HBV) and hepatitis C Virus (HCV) prevalence and for development of hepatocellular carcinoma subsequent to HBV and/or HCV infection (25). ...
Inflammation is an integral part of defense against most infectious diseases. These pathogen-induced immune responses are in very many instances strongly influenced by host’s sex. As a consequence, sexual dimorphisms were observed in susceptibility to many infectious diseases. They are pathogen dose-dependent, and their outcomes depend on pathogen and even on its species or subspecies. Sex may differentially affect pathology of various organs and its influence is modified by interaction of host’s hormonal status and genotype: sex chromosomes X and Y, as well as autosomal genes. In this Mini Review we summarize the major influences of sex in human infections and subsequently focus on 22 autosomal genes/loci that modify in a sex-dependent way the response to infectious diseases in mouse models. These genes have been observed to influence susceptibility to viruses, bacteria, parasites, fungi and worms. Some sex-dependent genes/loci affect susceptibility only in females or only in males, affect both sexes, but have stronger effect in one sex; still other genes were shown to affect the disease in both sexes, but with opposite direction of effect in females and males. The understanding of mechanisms of sex-dependent differences in the course of infectious diseases may be relevant for their personalized management.
... Male children under age four had significantly more occurrences of measles, viral meningitis, and hepatitis infections [53]. Male sex in adults was also a significant predictor of severe disease outcome with several viruses, including from hepatitis A, hepatitis B, Epstein-Barr virus, and West Nile virus [54][55][56][57][58]. Men also had higher CD8 + T cells [12,[15][16][17] NK cells [12,[15][16][17] B cells and IgM [10][11][12] neutrophils [13,14] [ [18][19][20][21] TLR7: in females [77,[79][80][81]131] TLR8: in females [52] ACE2: in females [48] ACE2 (ES ) [100] TMPRSS2 (TS) [101] IFN (ES) [18][19][20][21] BTK: in females [126,127] CD40L: in females [123][124][125] CXCR3: in females [130,140] IFN [26][27][28] Treg function (ES) levels of HIV RNA in their blood, although when accounting for viral load, women were more likely to develop AIDS [59]. ...
Females have more robust immune responses than males, and viral infections are more severe for males. Hormones and genetic sex, namely the X chromosome, influence sex differences with immune responses. Here, we review recent findings underlying sexual dimorphism of disease susceptibility for two prevalent viral infections, influenza and SARS-CoV-2, which exhibit male-biased disease severity. Viral infections are proposed to be an initiating event for autoimmunity, which exhibits a female bias. We also review recent work elucidating the epigenetic and genetic contribution of X-Chromosome Inactivation maintenance, and X-linked gene expression, for the autoimmune disorder Systemic Lupus Erythematosus, and highlight the complex considerations required for identifying underlying hormonal and genetic contributions responsible for sex differences in immune responses.
... Contrary to prior studies, we did not find coinfection (with HBV or HCV) to be associated with hepatitis A-related hospitalization [4,10,[22][23][24]. It is possible that our classification scheme (evidence of past or current HBV or HCV infection) played a role in the lack of evidence of an association between HBV or HCV coinfection and hospitalization in our study; however, we assessed active, current HCV infection via quantifiable HCV ribonucleic acid viral load, and the association with hospitalization was not statistically significant. ...
Background:
Since 2016, the US has experienced person-to-person hepatitis A outbreaks unprecedented in the vaccine era. The proportion of cases hospitalized in these outbreaks exceeds historical national surveillance data.
Methods:
We described the epidemiology, characterized the reported increased morbidity, and identified factors associated with hospitalization during the outbreaks by reviewing a 10% random sample of outbreak-associated hepatitis A cases in Kentucky, Michigan, and West Virginia-three heavily affected states. We calculated descriptive statistics and conducted age-adjusted log-binomial regression analyses to identify factors associated with hospitalization.
Results:
Participants in the random sample (n=817) were primarily male (62.5%) with mean age of 39.0 years; 51.8% were hospitalized. Among those with available information, 73.2% reported drug use, 14.0% were experiencing homelessness, 29.7% were currently or recently incarcerated, and 61.6% were epidemiologically linked to a known outbreak-associated case. Residence in Michigan (adjusted risk ratio [aRR] 1.8), being a man who has sex with men (aRR 1.5), non-injection drug use (aRR 1.3), and homelessness (aRR 1.3) were significantly (p<0.05) associated with hepatitis A-related hospitalization.
Conclusions:
Our findings support current Advisory Committee on Immunization Practices recommendations to vaccinate all persons who use drugs, men who have sex with men, and persons experiencing homelessness against hepatitis A.
... Acute cases were high prevalent among males and those aging more than 40 years, where the disease is more severe. A study of hospitalization due to HAV in Taiwan found overall mortality rate of 16.8 per 1000 hospitalizations where high fatality rates was found in males and adjusted odds ratio for death rose by age and increased rapidly over 40 years of age [31]. Some studies showed that fatal cases occurred in individuals aging more than 40 years [32,33]. ...
Objectives:
Little is known about hepatitis A virus (HAV) prevalence in indigenous communities. This study aims to evaluate the prevalence of HAV in indigenous community compared to urban population located at Western Amazon in Brazil.
Results:
A total of 872 serum samples were obtained from 491 indigenous and 381 non indigenous individuals aging 0 to 90 years. Samples were tested for total and IgM anti-HAV and positive IgM samples were tested for HAV RNA. The overall prevalence of total anti-HAV was 87%, increased according age showing 100% of prevalence in those aging more than 30 years (p < 0.0001) and it was similar among indigenous and urban population. Total anti-HAV prevalence varied between tribes (p < 0.0001) and urban sites (p = 0.0014) and spatial distribution showed high prevalence in homes that received up to 100 dollars. IgM anti-HAV prevalence was 1.7% with predominance in males, those aging more than 41 years. No HAV RNA was detected. In conclusion, high overall anti-HAV prevalence was found in indigenous communities in North Brazil demonstrating the importance of universal vaccination in this group.
