• CCAAT enhancer binding protein beta
• ORF6
• PRRSV
• miR-320
• pig

• Animals
• CCAAT-Enhancer-Binding Protein-beta/metabolism
• CCAAT-Enhancer-Binding Protein-beta/genetics
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Porcine Reproductive and Respiratory Syndrome/genetics
• Porcine Reproductive and Respiratory Syndrome/virology
• Porcine respiratory and reproductive syndrome virus/genetics
• Porcine respiratory and reproductive syndrome virus/physiology
• Swine
• Virus Replication
• Viral Proteins/genetics
• Viral Proteins/metabolism

• 2021YFD1301201 National Key Research and Development Program of China
• 2021-620-000-001-030 Agricultural Science Innovation Foundation of Hubei Province
• 2022AB015 Science and Technology Project of Xinjiang Production and Construction Corps

• HBV
• TLR7
• interleukin
• pregnancy

• Female
• Humans
• Pregnancy
• DNA, Viral
• Hepatitis B
• Hepatitis B e Antigens
• Hepatitis B Surface Antigens
• Hepatitis B virus
• Infectious Disease Transmission, Vertical
• Interleukin-3
• Interleukin-6/genetics
• Pregnancy Complications, Infectious
• Toll-Like Receptor 7/genetics
• Infant, Newborn

• Biomarker
• Diagnosis
• Hepatitis B virus
• Hepatocellular carcinoma
• MicroRNA
• Prognosis

• Humans
• MicroRNAs/genetics
• Carcinoma, Hepatocellular/diagnosis
• Carcinoma, Hepatocellular/genetics
• Hepatitis B virus/genetics
• Liver Neoplasms/diagnosis
• Liver Neoplasms/genetics
• Prognosis
• Biomarkers
• Hepatitis B/complications
• Hepatitis B/diagnosis

• Immunity
• Inflammation
• Liver diseases
• Tumorigenesis
• miR-155

• diagnostic markers
• exosomes
• intercellular communication
• liver pathologies
• microRNAs
• therapeutic targets

Over time, more and more is becoming known about micro-players of great significance. This is particularly the case for microRNAs (miRNAs; miR), which have been found to participate in the regulation of many physiological and pathological processes in both humans and animals. One such process is viral infection in humans and animals, in which the host miRNAs—alone or in conjunction with the virus—interact on two levels: viruses may regulate the host’s miRNAs to evade its immune system, while the host miRNAs can play anti- or pro-viral roles. The purpose of this comprehensive review is to present the key miRNAs involved in viral infections in humans and animals. We summarize the data in the available literature, indicating that the signature miRNAs in human viral infections mainly include 12 miRNAs (i.e., miR-155, miR-223, miR-146a, miR-122, miR-125b, miR-132, miR-34a, miR -21, miR-16, miR-181 family, let-7 family, and miR-10a), while 10 miRNAs are commonly found in animals (i.e., miR-155, miR-223, miR-146a, miR-145, miR-21, miR-15a/miR-16 cluster, miR-181 family, let-7 family, and miR-122) in this context. Knowledge of which miRNAs are involved in different viral infections and the biological functions that they play can help in understanding the pathogenesis of viral diseases, facilitating the future development of therapeutic agents for both humans and animals.

• Lagovirus europaeus/RHDV
• Marek’s disease virus
• foot-and-mouth disease virus
• hemorrhagic viruses
• hepatitis viruses
• microRNA
• porcine reproductive and respiratory syndrome virus
• rabies virus
• respiratory viruses
• viral infections

• Antiviral immunity
• MicroRNA-155
• Pathogenesis
• T cells
• Viral infections

Genetic variants in microRNAs (miRNAs) can alter the miRNAs expression and/or function, accordingly, affecting the related biological pathways and disease risk. Dysregulation of miR-155 and miR-146a expression levels has been well-described in viral hepatitis B (HBV). In the current study, we aimed to assess rs767649 T/A and rs57095329 A/G polymorphisms in miR-155, and miR-146a genes, respectively, as risk factors for Chronic HBV (CHBV) in the Egyptian population. Also, we aimed to do in silico analysis to investigate the molecules that primarily target these miRNAs. One hundred patients diagnosed as CHBV and one hundred age and sex-matched controls with evidence of past HBV infection were genotyped for miR-155 (rs767649) and miR-146a (rs57095329) using real-time polymerase chain reaction. The rs767649 AT and AA genotypes in CHBV patients confer four folds and ten folds risk respectively, as compared to control subjects [(AOR = 4.245 (95%CI 2.009–8.970), p<0.0001) and AOR = 10.583 (95%CI 4.012–27.919), p<0.0001, respectively)]. The rs767649 A allele was associated with an increased risk of developing CHBV (AOR = 2.777 (95%CI 1.847–4.175), p<0.0001). There was a significant difference in the frequency of rs57095329 AG and GG genotypes in CHBV patients compared to controls. AG and GG genotypes showed an increase in the risk of developing CHBV by about three and six folds respectively [AOR = 2.610 (95%CI 1.362–5.000), p = 0.004] and [AOR = 5.604 (95%CI 2.157–14.563), p<0.0001].We concluded that rs57095329 and rs767649 SNPs can act as potential risk factors for the development of CHBV in the Egyptian population.

• Adult
• Alleles
• Egypt/epidemiology
• Female
• Gene Expression Regulation
• Genetic Association Studies
• Genetic Predisposition to Disease
• Genotype
• Hepatitis B virus/genetics
• Hepatitis B virus/pathogenicity
• Hepatitis B, Chronic/epidemiology
• Hepatitis B, Chronic/genetics
• Hepatitis B, Chronic/virology
• Humans
• Male
• MicroRNAs/genetics
• Polymorphism, Single Nucleotide/genetics
• Risk Factors

• hepatic ischemia/reperfusion
• hepatitis
• liver injury
• microRNA‑155

Background: Dysregulated immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are thought to underlie the progression of coronavirus disease 2019 (COVID-19). We sought to further characterize host antiviral and cytokine gene expression in COVID-19 patients based on illness severity.

Methods: In this case-control study, we retrospectively analyzed 46 recovered COVID-19 patients and 24 healthy subjects (no history of COVID-19) recruited from the Second People's Hospital of Fuyang City. Blood samples were collected from each study participant for RNA extraction and PCR. We assessed changes in antiviral gene expression between healthy controls and patients with mild/moderate (MM) and severe/critical (SC) disease.

Results: We found that type I interferon signaling (IFNA2, TLR8, IFNA1, IFNAR1, TLR9, IRF7, ISG15, APOBEC3G, and MX1) and genes encoding proinflammatory cytokines (IL12B, IL15, IL6, IL12A and IL1B) and chemokines (CXCL9, CXCL11 and CXCL10) were upregulated in patients with MM and SC disease. Moreover, we found that IFNA1, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G (APOBEC3G), and Fas-associated protein with death domain (FADD) were significantly downregulated (P < 0.05) in the SC group compared to the MM group. We also observed that microRNA (miR)-155 and miR-130a levels were markedly higher in the MM group compared to the SC group.

Conclusion: COVID-19 is associated with the activation of host antiviral genes. Induction of the IFN system appears to be particularly important in controlling SARS-CoV-2 infection, as decreased expression of IFNA1, APOBEC3G and FADD genes in SC patients, relative to MM patients, may be associated with disease progression.

• APOBEC3G
• COVID-19
• IL6
• SARS-CoV-2
• immune response genes

• Alcohol
• Ethanol
• Insulin resistance
• Myocardium
• mTOR
• miR-155

• CEBPB
• GLI
• GPR39
• HBV
• HCC
• HSP

• CCAAT-Enhancer-Binding Protein-beta/metabolism
• Heat-Shock Proteins/metabolism
• Heat-Shock Response
• Hedgehog Proteins/metabolism
• Hep G2 Cells
• Hepatitis B virus/physiology
• Humans
• Models, Biological
• RNA Interference
• Receptors, G-Protein-Coupled/metabolism
• Signal Transduction
• Virus Replication

Circulating microRNAs (miRNAs) have been shown to dysregulate in many cancer types including hepatocellular carcinoma (HCC). The purpose of this study was to examine the potential diagnostic or prognostic roles of circulating miRNAs in patients with hepatitis B virus (HBV)-related HCC.

Paired cancerous and adjacent non-cancerous liver tissue specimens of patients with HBV-related HCC were used as a discovery set for screening 800 miRNAs by a Nanostring quantitative assay. Differentially expressed miRNAs were then examined by SYBR green quantitative RT-PCR in a validation cohort of serum samples obtained from 70 patients with HBV-related HCC, 70 HBV patients without HCC and 50 healthy controls.

The discovery set identified miR-223-3p, miR-199a-5p and miR-451a significantly lower expressed in cancerous tissues compared with non-cancerous tissues. In the validated cohort, circulating miR-223-3p levels were significantly lower in the HCC group compared with the other groups. The combined use of serum alpha-fetoprotein and miR-223-3p displayed high sensitivity for detecting early HCC (85%) and intermediate/advanced stage HCC (100%). Additionally, serum miR-223-3p had a negative correlation with tumor size and BCLC stage. On multivariate analysis, serum miR-223-3p was identified as an independent prognostic factor of overall survival in patients with HCC. In contrast, circulating miRNA-199a-5p and miR-451a did not show any clinical benefit for the diagnosis and prognostic prediction of HCC.

Our results demonstrated that miR-223-3p was differentially expressed in cancerous compared with paired adjacent non-cancerous tissues. In addition, circulating miRNA-223-3p could represent a novel diagnostic and prognostic marker for patients with HBV-related HCC.

• Biomarkers, Tumor/genetics
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/virology
• Case-Control Studies
• Circulating MicroRNA/genetics
• Female
• Gene Expression Regulation, Neoplastic/genetics
• Hepatitis B virus/pathogenicity
• Hepatitis B, Chronic/genetics
• Hepatitis B, Chronic/pathology
• Hepatitis B, Chronic/virology
• Humans
• Liver Neoplasms/genetics
• Liver Neoplasms/pathology
• Liver Neoplasms/virology
• Male
• MicroRNAs/genetics
• Middle Aged
• Prognosis

• Thailand Research Fund
• Chulalongkorn University
• Royal Golden Jubilee (RGJ) Ph.D. Programme

The World Health Organisation, in its 2019 progress report on HIV, viral hepatitis and STDs indicates that 257 million people are afflicted with chronic HBV infections, of which, 1 million patients lose their lives every year due to HBV related chronic liver diseases including serious complications such as liver cirrhosis and hepatocellular carcinoma. The course of HBV infection and associated liver injury depend on several host factors, genetic variability of the virus, and the host viral interplay. The challenge of medical science is the early diagnosis/identification of the potential for development of fatal complications like liver cirrhosis and HCC so that timely medical intervention can improve the chances of survival. Currently, neither the vaccination regime nor the diagnostic methods are completely effective as reflected in the high number of annual deaths. It is evident from numerous publications that microRNAs (miRNAs) are the critical regulators of gene expression and various cellular processes like proliferation, development, differentiation, apoptosis and tumorigenesis. Expressions of these diminutive RNAs are significantly affected in cancerous tissues as a result of numerous genomic and epigenetic modifications. Exosomes are membrane-derived vesicles (30–100 nm) secreted by normal as well as malignant cells, and are present in all body fluids. They are recognized as critical molecules in intercellular communication between cells through horizontal transfer of information via their cargo, which includes selective proteins, mRNAs and miRNAs. Exosomal miRNAs are transferred to recipient cells where they can regulate target gene expression. This provides an insight into the elementary biology of cancer progression and therefore the development of therapeutic approaches. This concise review outlines various on-going research on miRNA mediated regulation of HBV pathogenesis with special emphasis on association of exosomal miRNA in advanced stage liver disease like hepatocellular carcinoma. This review also discusses the possible use of exosomal miRNAs as biomarkers in the early detection of HCC and liver cirrhosis.

• Exosome
• Hepatitis B virus
• Hepatocellular carcinoma
• miRNA

Duck hepatitis A virus type 3 (DHAV-3) is one of the most harmful pathogens in the duck industry. However, the molecular mechanism underlying DHAV-3 infection in ducklings remains poorly understood. To study the genetic regulatory network for miRNA-mRNA and the signaling pathways involved in DHAV-3 infection in ducklings, we conducted global miRNA and mRNA expression profiling of duckling liver tissues infected with lethal DHAV-3 by high-throughput sequencing.

We found 156 differentially expressed miRNAs (DEMs) and 7717 differentially expressed genes (DEGs) in livers of mock-infected and DHAV-3-infected duckling. A total of 19,606 miRNA-mRNA pairs with negatively correlated expression patterns were identified in miRNA-mRNA networks constructed on the basis of these DEMs and DEGs. Moreover, immune-related pathways, including the cytokine-cytokine receptor interaction, apoptosis, Toll-like receptor, Jak-STAT, and RIG-I-like receptor signaling pathway, were significantly enriched through analyzing functions of mRNAs in the network in response to DHAV-3 infection. Furthermore, apl-miR-32-5p, apl-miR-125-5p, apl-miR-128-3p, apl-miR-460-5p, and novel-m0012-3p were identified as potential regulators in the immune-related signaling pathways during DHAV-3 infection. And some host miRNAs were predicted to target the DHAV-3 genome.

This is the first integrated analysis of miRNA and mRNA in DHAV-3-infected ducklings. The results indicated the important roles of miRNAs in regulating immune response genes and revealed the immune related miRNA-mRNA regulation network in the DHAV-3-infected duckling liver. These findings increase our knowledge of the roles of miRNAs and their target genes in DHAV-3 replication and pathogenesis. They also aid in the understanding of host-virus interactions.

• Duck hepatitis a virus type 3
• Host-virus interactions
• Innate immune response
• Transcriptome
• miRNA
• miRNA-mRNA network

The hepatitis B virus (HBV) chronically infects over 250 million people worldwide and is one of the leading causes of liver cancer and hepatocellular carcinoma. HBV persistence is due in part to the highly stable HBV minichromosome or HBV covalently closed circular DNA (cccDNA) that resides in the nucleus. As HBV replication requires the help of host transcription factors to replicate, focusing on host protein–HBV genome interactions may reveal insights into new drug targets against cccDNA. The structural details on such complexes, however, remain poorly defined. In this review, the current literature regarding host transcription factors’ interactions with HBV cccDNA is discussed.

• covalently closed circular DNA (cccDNA)
• hepatitis B virus (HBV)
• host–viral interactions
• transcription factors
• viral replication

• HBV replication
• SOCS1
• autophagy
• infection
• miR-155

• acute liver injury
• biomarker
• cirrhosis
• microRNAs
• murine models
• patients.

• HBV
• HCV
• cirrhosis
• hepatocellular carcinoma

• HBV
• HCV
• cirrhosis
• hepatocellular carcinoma

MicroRNAs (miRNAs) function as crucial suppressors of gene expression via translational repression or direct mRNA degradation. However, the mechanism of multi-gene regulation by a host miRNA in antiviral immunity has not been extensively explored. In this study, the regulation of two white spot syndrome virus (WSSV) genes by its host (Marsupenaeus japonicus shrimp) miRNA (shrimp miR-1000) was characterized. The miRNA target gene prediction showed that only two virus genes (wsv191 and wsv407) might be the targets of miR-1000. The results of insect cell transfection assays revealed that shrimp miR-1000 could target multiple virus genes (wsv191 and wsv407). The mRNA degradation analysis and RNA FISH (fluorescence in situ hybridization) analysis indicated that miR-1000 triggered the mRNA degradation of target genes through 5′-3′ exonucleolytic digestion in vivo and thereby inhibited the virus infection in shrimp. The miRNA-mediated 5′-3′ exonucleolytic digestion of target mRNAs stopped near the 3′UTR (3′untranslated region) sequence complementary to the seed sequence of miR-1000. Therefore, our study provided novel insights into how a host miRNA targeted multiple viral genes and prevented host from virus infection.

• mRNA degradation
• shrimp miR-1000
• virus-host interactions
• white spot syndrome virus gene
• wsv191 and wsv407

• Hepatocyte
• Human
• Liver Disease
• Pro-Inflammatory Cytokines
• microRNA

• cancer stem cells
• cell signaling
• epithelial-mesenchymal transition
• inflammation
• microRNAs

• chronic hepatitis B
• miR-155
• natural killer cells
• suppressor of cytokine signaling 1
• telbivudine

Noninvasive methods to accurately and conveniently evaluate liver fibrosis are desirable. MicroRNA (miR) is one of the candidates. MiRs are small RNAs consisting of 19–25 nucleotides that negatively regulate many target genes at transcriptional levels. Recently, many researchers have focused on circulating miRs in the blood stream as biomarkers. Hepatic miR-122 has been reported to have an association with viral replication and hepatic fibrosis in chronic hepatitis B virus (HBV) and hepatic C virus (HCV) infection.

We measured serum miR-122 levels in HBV- and HCV-infected patients confirmed with liver biopsy. We also investigated a novel liver fibrosis marker Wisteria floribunda agglutinin-positive Mac-2 binding protein [WFA(+)-M2BP]. We evaluated the diagnostic usefulness of these markers in hepatic fibrosis and inflammation of patients with chronic viral infection.

The serum miR-122 levels of HBV-infected patients were higher than those of the control subjects. In HBV-infected patients, the serum miR-122 levels of patients with advanced liver fibrosis were significantly lower. Serum WFA(+)-M2BP was significantly higher dependent on both the staging of fibrosis and the grading of inflammatory activity in patients with both HBV and HCV infection. We also observed that higher serum WFA(+)-M2BP levels augmented the prediction of advanced liver fibrosis among HBV-infected patients with lower serum miR-122 levels.

A lower serum miR-122 level is a useful predictor of advanced liver fibrosis in HBV-infected patients. Serum WFA(+)-M2BP could predict liver fibrosis in both HBV and HCV infection. The combination of these markers may result in the more accurate evaluation of liver fibrosis in HBV infection.

Toll like receptors (TLRs) play an important role in innate immunity and various studies suggest that TLRs play a crucial role in pathogenesis of hepatitis B virus (HBV) infection. The present study aims in looking into the status of crucial host and viral gene expression on inciting TLR7.

The transcription of TLR7 pathway signaling molecules and HBV DNA viral load were quantified by Real Time-PCR after stimulation of TLR7 with its imiquimod based ligand, R837. Cell cycle analysis was performed using flow-cytometry. Expression of TLR7 and chief cell cycle regulator governing G1/S transition, p53 was also seen in liver biopsysss samples of CHB patients. HBV induced alteration in histone modifications in HepG2 cells and its restoration on TLR7 activation was determined using western blot.

The TLR7 expression remains downregulated in HepG2.2.15 cells and in liver biopsy samples from CHB patients. Interestingly HBV DNA viral load showed an inverse relationship with the TLR7 expression in the biopsy samples. We also evaluated the anti-viral activity of R837, an agonist of TLR7. It was observed that there was a suppression of HBV replication and viral protein production upon TLR7 stimulation. R837 triggers the anti-viral action probably through the Jun N-terminal Kinase (JNK) pathway. We also observed a downregulation of histone H3K9Me3 repression mark upon R837 treatment in HBV replicating HepG2.2.15 cells, mimicking that of un-infected HepG2 cells. Additionally, the G1/S cell cycle arrest introduced by HBV in HepG2.2.15 cells was released upon ligand treatment.

The study thus holds a close insight into the changes in hepatocyte micro-environment on TLR7 stimulation in HBV infection.

The online version of this article (doi:10.1186/s12879-017-2189-z) contains supplementary material, which is available to authorized users.

• Cell-cycle arrest
• Epigenetics
• Hepatitis B virus
• Innate immune response
• TLR7

• HBV replication
• cell metabolism
• hepatocytes
• microRNA
• transcription factors

Toll like receptors plays a significant anti-viral role in different infections. The aim of this study was to look into the role of toll like receptor 4 (TLR4) in hepatitis B virus (HBV) infection.

Real time PCR was used to analyze the transcription of TLR4 signaling molecules, cell cycle regulators and HBV DNA viral load after triggering the HepG2.2.15 cells with TLR4 specific ligand. Nuclear factor (NF)-κB translocation on TLR4 activation was analyzed using microscopic techniques. Protein and cell cycle analysis was done using Western Blot and FACS respectively.

The present study shows that TLR4 activation represses HBV infection. As a result of HBV suppression, there are several changes in host factors which include partial release in G1/S cell cycle arrest and changes in host epigenetic marks. Finally, it was observed that anti-viral action of TLR4 takes place through the NF-κB pathway.

The study shows that TLR4 activation in HBV infection brings about changes in hepatocyte microenvironment and can be used for developing a promising therapeutic target in future.

• Hepatitis B virus
• Toll like receptor 4
• Cell cycle
• Epigenetic marks
• Innate immune response

• Active Transport, Cell Nucleus
• Cellular Microenvironment
• DNA Methylation
• DNA, Viral/genetics
• Dose-Response Relationship, Drug
• Epigenesis, Genetic
• G1 Phase Cell Cycle Checkpoints
• Hep G2 Cells
• Hepacivirus/genetics
• Hepacivirus/pathogenicity
• Hepatitis B, Chronic/genetics
• Hepatitis B, Chronic/metabolism
• Hepatitis B, Chronic/prevention & control
• Hepatitis B, Chronic/virology
• Hepatocytes/drug effects
• Hepatocytes/metabolism
• Hepatocytes/virology
• Host-Pathogen Interactions
• Humans
• Ligands
• Lipopolysaccharides/pharmacology
• NF-kappa B/metabolism
• Signal Transduction
• Time Factors
• Toll-Like Receptor 4/agonists
• Toll-Like Receptor 4/genetics
• Toll-Like Receptor 4/metabolism
• Viral Load

• Gerotarget
• inflamm-aging
• microRNA
• senescence
• senescence-associated secretory phenotype

• HBV
• NFIA
• miR-370
• microRNA
• viral gene expression

• Hepatitis B virus (HBV)
• Prolonged HBV infection
• TLR7

• Alanine Transaminase
• Hepatitis B, Chronic
• Immunity
• Leukocytes
• Mononuclear
• miR-155

Hepatitis B virus (HBV) infection is a major public health problem worldwide. HBV is not directly cytotoxic to infected hepatocytes; the clinical outcome of infection results from complicated interactions between the virus and the host immune system. In acute HBV infection, initiation of a broad, vigorous immune response is responsible for viral clearance and self-limited inflammatory liver disease. Effective and coordinated innate and adaptive immune responses are critical for viral clearance and the development of long-lasting immunity. Chronic hepatitis B patients fail to mount efficient innate and adaptive immune responses to the virus. In particular, HBV-specific cytotoxic T cells, which are crucial for HBV clearance, are hyporesponsiveness to HBV infection. Accumulating experimental evidence obtained from the development of animal and cell line models has highlighted the importance of innate immunity in the early control of HBV spread. The virus has evolved immune escape strategies, with higher HBV loads and HBV protein concentrations associated with increasing impairment of immune function. Therefore, treatment of HBV infection requires inhibition of HBV replication and protein expression to restore the suppressed host immunity. Complicated interactions exist not only between innate and adaptive responses, but also among innate immune cells and different components of adaptive responses. Improved insight into these complex interactions are important in designing new therapeutic strategies for the treatment HBV infection. In this review, we summarize the current knowledge regarding the cross-talk between the innate and adaptive immune responses and among different immunocytes in HBV infection.

• Crosstalk
• Hepatitis B virus
• Innate immune
• Adapative immune

Hepatitis B Virus (HBV) manifests high genetic variability and is classifiable into ten genotypes (A-J). HBV infection can lead to variable clinical outcomes, ranging from self-limiting acute hepatitis to active chronic hepatitis, cirrhosis and hepatocellular carcinoma. The present study characterizes HBV strains circulating among patients with acute (AHB) and chronic HBV infection (CHB). Among a total of 653 HBsAg positive cases, 40 manifested acute infection. After sequencing the surface(S), basal core promoter/pre-core(BCP/PC) and the X gene regions, phylogenetic tree was constructed using MEGA4 by neighbor-joining method. Statistical robustness was established with bootstrap analysis. Nucleotide diversity was determined by Shannon entropy per site using the Entropy program of the Los Alamos National Laboratories. Analyses of acute patients revealed that HBV/D2 is the major circulating sub-genotype and commonly associated with sexual promiscuity and the age group between15-30 years. Comparison of AHB and CHB patients revealed that HBeAg positivity, ALT levels and genotype D were significantly high in AHB, whereas CHB patients were predominantly male, had a high viral load, and were commonly associated with genotype C. The frequencies of mutations in the S, BCP/PC, and X gene were low in AHB as compared to CHB. Drug resistant mutations were not detectable in the polymerase gene of AHB. Average nucleotide diversity in AHB was considerably low as compared to CHB. Further, the highest average ΔH (average difference in entropy between chronic and acute infection) was observed in the BCP/PC region implying that this region was most vulnerable to mutations upon HBV persistence, especially in case of genotype C. Additionally, among all substitutions, the A1762T and G1764A BCP mutations were the strongest indicators of chronicity. In conclusion, the study exhibits a general portrait of HBV strains circulating among acute hepatitis B patients in Eastern India and their intricate differences with chronic patients which should be useful from the clinical point of view.

• Adolescent
• Adult
• DNA, Viral/genetics
• Female
• Genetic Variation
• Genotype
• Hepatitis B/epidemiology
• Hepatitis B/virology
• Hepatitis B Core Antigens/genetics
• Hepatitis B virus/genetics
• Hepatitis B, Chronic/epidemiology
• Hepatitis B, Chronic/virology
• Humans
• India
• Male
• Middle Aged
• Models, Statistical
• Molecular Sequence Data
• Mutation
• Nucleotides/genetics
• Phylogeny
• Promoter Regions, Genetic
• Viral Load
• Young Adult

Hepatitis B virus (HBV) attacks the liver and can cause both acute as well as chronic liver diseases which might lead to liver cirrhosis and hepatocellular carcinoma. Regardless of the availability of a vaccine and numerous treatment options, HBV is a major cause of morbidity and mortality across the world. Recently, microRNAs (miRNAs) have emerged as important modulators of gene function. Studies on the role of miRNA in the regulation of hepatitis B virus gene expression have been the focus of modern antiviral research. miRNAs can regulate viral replication and pathogenesis in a number of different ways, which includefacilitation, direct or indirect inhibition, activation of immune response, epigenetic modulation, etc. Nevertheless, these mechanisms can appropriately be used with a diagnosticand/or therapeutic approach. The present review is an attempt to classify specific miRNAs that are reported to be associated with various aspects of hepatitis B biology, in order to precisely present the participation of individual miRNAs in multiple aspects relating to HBV.

• HBV
• chronic
• hepatocellular carcinoma
• liver cirrhosis
• miRNA

• Animals
• Carcinoma, Hepatocellular/etiology
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/virology
• Hepatitis B/complications
• Hepatitis B/genetics
• Hepatitis B/metabolism
• Hepatitis B/virology
• Host-Pathogen Interactions/genetics
• Humans
• Liver Cirrhosis/etiology
• Liver Cirrhosis/genetics
• Liver Cirrhosis/metabolism
• Liver Cirrhosis/virology
• Liver Neoplasms/etiology
• Liver Neoplasms/genetics
• Liver Neoplasms/metabolism
• Liver Neoplasms/virology
• MicroRNAs/genetics