Steatotic liver disease (SLD) affects ~30% of adults worldwide. The global population is continuously threatened by epidemic and endemic viral diseases. This study aims to thoroughly examine the interaction between SLD and major viral diseases.

We systematically searched databases from inception to April 2, 2024, for observational studies recording viral-infected adult patients with eligible data on the presence of hepatic steatosis.

Six hundred thirty-six eligible studies were included in the analysis of SLD prevalence. Among patients with monoinfections, the highest SLD prevalence was observed in those infected with HCV at 49% (95% CI: 47%-51%), followed by SARS-CoV-2 (39%, 95% CI [34%-44%]), HIV (39%, 95% CI [33%-44%]), and HBV (36%, 95% CI [32%-40%]). Additionally, co-infections, such as HCV-HIV and HBV-HCV, exhibit even higher SLD prevalence. The prevalence of steatohepatitis is particularly high in HIV-infected (24%, 95% CI: 17%-30%) and HCV-infected (18%, 95% CI: 13%-24%) populations. The co-existence of SLD with viral infections was associated not only with the progression of liver disease but also with more severe outcomes of the infections and poorer responses to antiviral treatment. The combination of cardiometabolic risk factors and viral-associated and host factors contributes to the higher risk of SLD in viral-infected populations.

SLD is highly prevalent in viral-infected populations, and the reciprocal interactions between SLD and viral diseases exacerbate both conditions, leading to poorer patient outcomes in general.

Nonalcoholic fatty liver disease (NAFLD), first named in 1980, is currently the most common chronic liver disease, imposing significant health, social, and economic burdens. However, it is defined as a diagnosis of exclusion, lacking a clear underlying cause in its diagnostic criteria. In 2020, metabolic dysfunction-associated fatty liver disease (MAFLD) was proposed as a replacement for NAFLD, introducing additional criteria related to metabolic dysfunction. In 2023, metabolic dysfunction-associated steatotic liver disease (MASLD) was suggested to replace NAFLD, aiming to avoid the stigmatizing term "fatty" and incorporating cardiometabolic criteria for metabolic dysfunction. This divergence in nomenclature and diagnostic criteria between MAFLD and MASLD presents challenges to medical communication and progress. This review outlines the pros and cons of both terminologies, based on current research evidence, in the hope of fostering global consensus in the future.

Steatohepatitic hepatocellular carcinoma (SH-HCC) is currently recognized as a distinct histologic subtype of HCC. The prognosis and specific criteria for determining the amount of steatohepatitis required to define SH-HCC are still unclear.

After excluding all recognized HCC subtypes from 505 HCC cases (2010-2019), the remaining cases were categorized as conventional HCC (CV-HCC) (n = 223). The cases classified as SH-HCC (n = 171) were further divided into groups based on the percentage of steatohepatitis: 5% or more, 30% or more, and 50% or more.

Hepatitis C virus infection was the predominant underlying liver disease in both the CV-HCC and SH-HCC groups. Metabolic dysfunction-associated steatotic liver disease (formerly nonalcoholic fatty liver disease) was more prevalent in all cases of SH-HCC with different steatohepatitic cutoffs than in cases of CV-HCC. There were no differences in the stage of fibrosis of the background liver between the CV-HCC and SH-HCC groups. SH-HCC with different cutoffs exhibited a notable increase in the presence of glycogenated nuclei, Mallory-Denk bodies, and hyaline globules in tumor cells. Survival analysis did not reveal substantial differences in overall survival between the CV-HCC and SH-HCC groups and among patients with SH-HCC with different steatohepatitis cutoffs.

The degree of intratumoral steatohepatitis in patients with SH-HCC does not appear to be a notable prognostic factor. The presence of steatohepatitis in the tumor is better recognized as 1 of the histopathologic patterns of HCC.

Steatotic liver disease (SLD) is an emerging liver disease, whereas chronic viral hepatitis is the renowned cause of chronic liver disease leading to cirrhosis and hepatocellular carcinoma (HCC). The impact of coexisting SLD in chronic hepatitis B (CHB) on liver-related events (LREs) in the long term is still debated. This study aims to compare all-cause mortality and LRE between CHB patients with and without SLD. This retrospective study included CHB patients who underwent transient elastography between 2014 and 2021 at a tertiary-care hospital. Exclusion criteria were those without controlled attenuated parameter (CAP) results, interquartile range/median of liver stiffness measurement (LSM) > 30%, follow-up time < 6 months, and without hepatitis B virus DNA data during follow-up. SLD was defined as CAP ≥ 248 dB/m, significant liver fibrosis (SF) as LSM ≥ 7 kPa, and cirrhosis as LSM ≥11 kPa or imaging evidence. LRE was defined as the development of HCC and/or cirrhosis complications. Among 532 patients (median follow-up 4.3 years), SLD was present in 161 (30.2%) patients, SF was found in 186 (34.5%) patients, and 104 (19.6%) patients had cirrhosis at baseline. SF was insignificantly more common in SLD patients (40.1% vs 32.4%, P = 0.068). Long-term outcomes showed SF, not SLD, was independently associated with higher LRE development with an adjusted HR of 13.85 (95% confidence interval [CI]: 3.06-62.76, P < 0.001), while the adjusted HR of SLD was 0.49 (95% CI: 0.16-1.53, P = 0.22). In conclusion, SLD commonly coexists with CHB patients. CHB patients with SLD were more likely to have SF at baseline, albeit not significantly. Long-term HCC and cirrhosis complications development are associated with SF but not SLD status.

Effective antiretroviral therapy (ART) is now nearly ubiquitous. However, the survival benefits conferred with ART contribute to an aging human immunodeficiency virus (HIV) population and increased risk of chronic diseases, like atherosclerotic cardiovascular disease (ASCVD). Furthermore, HIV is a known risk enhancer of ASCVD and acknowledged as such in the current 2018 AHA/ACC Blood Cholesterol guidelines [1]. This makes cardiovascular risk factor identification and modification among people living with HIV (PLWH) of increasing importance to prevent cardiovascular events. In this review, we aim to summarize the epidemiology and pathogenesis of how HIV is linked to atherogenesis and to discuss cardiometabolic risk factor modification specific to PLWH, covering obesity, hypertension, insulin resistance, metabolic dysfunction-associated steatotic liver disease, and dyslipidemia.

Background: Chronic hepatitis B (CHB) and non-alcoholic fatty liver disease (NAFLD) are significant causes of chronic liver disease, potentially leading to liver cirrhosis and hepatocellular carcinoma. Moreover, the coexistence of CHB and NAFLD is increasingly common, although the relationship between NAFLD and inactive CHB infection remains poorly understood. Objectives: This study aimed to investigate the prevalence of NAFLD among patients with inactive CHB, identify risk factors for NAFLD, and determine predictors of significant fibrosis in these patients. Methods: This single-center cross-sectional study targeted patients with inactive CHB at Sultan Qaboos University Hospital from January 2010 to November 2021. Results: A total of 425 patients with inactive CHB were identified, of which 53.1% were male and 62.6% were aged 40-60 years. The prevalence of NAFLD was 47.8%. Various independent factors were associated with NAFLD, including type 2 diabetes mellitus, elevated low-density lipoprotein levels, high hemoglobin levels, low platelet counts, and normal alpha-fetoprotein levels. Significant associations were noted between NAFLD and significant fibrosis, with 10.5% of CHB patients with NAFLD exhibiting significant fibrosis compared to 1.4% of those without NAFLD. Other significant parameters included male gender, increased age, high alanine transaminase levels, elevated hemoglobin, and decreased platelet levels. Conclusions: The high prevalence of NAFLD in patients with inactive CHB and its associations with increased fibrosis and cirrhosis risk underscore the need for comprehensive management strategies for these patients.

Hepatocellular carcinoma (HCC) is a serious neoplastic disease with increasing incidence and mortality, accounting for 90% of all liver cancers. Hepatitis viruses are the major causative agents in the development of HCC. Hepatitis A virus (HAV) primarily causes acute infections, which is associated with HCC to a certain extent, as shown by clinicopathological studies. Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infections lead to persistent liver inflammation and cirrhosis, disrupt multiple pathways associated with cellular apoptosis and proliferation, and are the most common viral precursors of HCC. Mutations in the HBV X protein (HBx) gene are closely associated with the incidence of HCC, while the expression of HCV core proteins contributes to hepatocellular lipid accumulation, thereby promoting tumorigenesis. In the clinical setting, hepatitis D virus (HDV) frequently co-infects with HBV, increasing the risk of chronic hepatitis. Hepatitis E virus (HEV) usually causes acute infections. However, chronic infections of HEV have been increasing recently, particularly in immuno-compromised patients and organ transplant recipients, which may increase the risk of progression to cirrhosis and the occurrence of HCC. Early detection, effective intervention and vaccination against these viruses may significantly reduce the incidence of liver cancer, while mechanistic insights into the interplay between hepatitis viruses and HCC may facilitate the development of more effective intervention strategies. This article provides a comprehensive overview of hepatitis viruses and reviews recent advances in research on aberrant hepatic immune responses and the pathogenesis of HCC due to viral infection.