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The effect of high HBV load on both HCC risk and recurrence estimated in our meta-analyses would
encourage the use of anti-viral therapy for both chronic hepatitis B and HCC patients to reduce HBV
DNA level, aiming to decrease the incidence rate of HCC and improve the prognosis of HCC
patients. New virological tools for screening, diagnosis and monitoring of hepatitis b and c in
resource-limited settings. Acute infections in adults, whether symptomatic or otherwise, usually are
self-limited, characterized by viral clearance from the blood and liver and lasting immunity to
reinfection. It has been recommended that properly screened blood, using a reliable method like
ELISA. Extrahepatic manifestations of hepatitis c: A meta-analysis of prevalence, quality of life, and
economic burden. The presence of HBsAg in the blood is the first sign of viral infection, followed by
a surge in anti-HBc within the first two weeks of the appearance of HBsAg, waning by six months.
HCV-NS5A promotes virus replication by associating with Raf-1 kinase. HCV-induced oncogenic
signaling During the progression of liver disease to HCC, many common mutations occur, resulting
in the conversion of normal cells to tumorigenic cells. It has been reported that more than 90% of
HCV-induced liver cancer is due to the dysregulation of a complex epigenetic network ( 7 ). Since
the morbidity of HCC is relatively low among general population, the OR extracted from case-
control studies is pretty close to RR. Article types Author guidelines Editor guidelines Publishing
fees Submission checklist Contact editorial office Frontiers in Oncology. For the second vaccine, the
human volunteers show a broad and strong HCV-specific T-cell response ( 28, 63, 64 ). The higher
value is associated with a higher risk of cirrhosis development ( 17 ). HCV core protein-induced
ROS damages the host cell and accumulates the genetic variation, leading to cancer ( 23, 24 ). Wu
WYY, Kang KH, Chen SLS, Chiu SYH, Yen AMF, Fann JCY, et al. The copyright and other
intellectual property rights in this document are owned by CADTH and its licensors. An autopsy is
performed and a microscopic view of the. Immunotherapy in melanoma: recent advances and future
directions. AJanssen Global Services, LLC, Raritan, NJ, USA; CDRG Abacus, Manchester, UK;
NBarts and The London School of Medicine and Dentistry, London, UK. Only 1 HBV infected
patients (9%) achieved partial response status while 25% had an objective response in total
population ( 66 ). Viral pathogenesis and neurological disorders There are many mechanisms known
and hypothesized for the role of HCV in the occurrence and development of neurological and
psychiatric symptoms. The association of HCV in the development of neurological disorders has been
presented in Table 2. A significant increase was observed in hepatic steatosis and a reduction in
fibrosis score after the eradication of the virus by DAAs. HCV-induced fibrosis has been observed
more in HIV-coinfected patients than in mono-infected patients ( 52, 53 ). We need to increase
recognition of this very important disease. HCV infection frequently results in acute and chronic
cerebral vasculopathy. Mathew S, Ali A, Abdel-Hafiz H, Fatima K, Suhail M, Archunan G, et al.
Accreditation of this program does not imply endorsement by either Medscape, LLC or ANCC.
Additionally, ischemic events can cause non-cryo-bobulinemic vasculitis and systemic vasculitis (
75, 99, 100 ). Role of transforming growth factor-beta signaling in cancer. Of note, combined
positive score (CPS) used for assessing not only tumor cells' PD-L1 expression but also those in
immune cells, was significantly related to ORR and progression-free survival in this study ( 60 ).
The other mechanism hypothesized, based on an observational study by Wu et al. Molecular
mechanisms of viral hepatitis induced hepatocellular carcinoma. Hepatitis b genotype c correlated
with poor surgical outcomes for hepatocellular carcinoma. Circulatory shock Cardiogenic Shock
Hypovolemic Shock Sepsis, Septic Shock an. Neuroimaging findings in chronic hepatitis c virus
infection: Correlation with neurocognitive and neuropsychiatric manifestations. Hepatitis B virus
reactivation in cancer patients with positive Hepatitis B surface antigen undergoing PD-1 inhibition.
Molecular mechanism of hcv induced hcc Viral proteins play an important role in chronic infection.
Negative hepatitis b envelope antigen predicts intrahepatic recurrence in hepatitis b virus-related
hepatocellular carcinoma after ablation therapy. Recently, autologous T cells were engineered to
express TCR-specific epitopes from integrated HBV DNA in order to achieve antitumor efficacy in
HBV-associated HCC. The patient's ages ranged (0-70) years amongst male and female. Of the
noninvasive methods, liver stiffness measurement by transient elastography and serum biomarkers of
liver fibrosis are most common because of their relatively high diagnostic accuracy. This disease is
generally transmitted through exposure to infected body fluids. Authier FJ, Bassez G, Payan C,
Guillevin L, Pawlotsky JM, Degos JD, et al. In HBV-related HCC, data from high-throughput
sequencing (HTS) technology showed that TCR diversity in tumors was higher than in adjacent non-
tumor tissues. During chronic infection, the immune responses are significantly impaired. In addition,
it increases lipid peroxidation and disrupts mitochondrial function by altering the double-layer
lipoprotein of the mitochondrial membrane ( 22, 23 ). Symptomatic CHB patients, on the other hand,
have abnormal liver function and histologic features. In the host adaptive immune response to acute
HCV infection, the activation of response is observed several weeks after the HCV infection. Based
on the data generated from retrospective and prospective studies, the clinical manifestation of HCV
infection leads to many conditions such as lacunar syndrome, cardiovascular risk factors, and
bleeding ( 67, 95 ). In acute HBV infection, viremia is spontaneously resolved by the host’s immune
response, and manifested as seroconversion to anti-HBe and lack of HBsAg and HBeAg.
Approximately 50% of infected patients develop fatigue, which indicates chronic HCV infection.
The virus causes both acute and chronic hepatitis, including liver cirrhosis and the development of
cancer. PD-L1 expression level is commonly higher in HBV-related HCC, and the predictive effect of
PD-L1 expression requires investigation in HBV-related cohorts. The prevention of HCV infection
and transmission by protective vaccinations is urgently needed to protect the global population as
well as to reduce the occurrence of neurological disorders. Parkinson's disease and pesticides: A
meta-analysis of disease connection and genetic alterations. As a primary endpoint, consistent effect
on overall survival was also observed in advanced HCC with nivolumab and seemingly profitted
more in predefined subgroup of HBV infection ( 56 ). These immunoglobulins can be re-dissolved at
high temperatures. It provides a vast knowledge on the subject to the researcher. But these NK cells
have a high level of NKG2A inhibitory molecule, which further predisposes them to viral chronicity.
The expression of natural killer group 2, member A (NKG2A), blunted the activation of dendritic
cells on the surface of NK cells infected with HCV ( 1 ).
Neurological disorders are associated with the inflammatory responses of many cells, including
microglia and astrocytes. Appendix 7, Summary of Natural History, Diagnosis, Management, and
Prognosis of HBV. Chronic viral hepatitis induced by hepatitis C but not hepatitis B virus infection
correlates with increased liver angiogenesis. The AFP is present in three different forms, known as
AFP-L1, AFP-L2, and AFP-L3. Hepatitis c virus-related central and peripheral nervous system
disorders. Feasibility and safety of nivolumab in advanced hepatocellular carcinoma: real-life
experience from three German centers. Based on a recent study, it has been observed that
neurological and psychiatric symptoms develop in patients with non-cirrhosis symptoms without
significant correlation with the virus replication rate and liver disease severity ( 6 ). It will help them
in writing an effective research paper, dissertations, and thesis. The role and association of HCV
infection in the inflammatory diseases of the CNS is well known. Please share few words with us by
writing your suggestions, feedbacks, and queries in the comment box. They were screened for
Hepatitis B surface antigen (HBs Ag) and anti Hepatitis C (Anti HCV) by Enzyme Linked
Immunosorbent Assay (ELISA). HCV core protein-induced ROS damages the host cell and
accumulates the genetic variation, leading to cancer ( 23, 24 ). Wu WYY, Kang KH, Chen SLS, Chiu
SYH, Yen AMF, Fann JCY, et al. Moreover, the clarification of the detailed relationship will provide
valuable clues to elucidate the important roles of the HBV DNA level in hepatocarcinogenesis.
Development and clinical validation of the genedrive point-of-Care test for qualitative detection of
hepatitis c virus. Micro2. A hepatitis panel is ordered for a 27-year-old woman as part of a routine
work-. While the Southeast Asian cohort study showed that HCV genotype 6 is strongly associated
with HCC development. HCV causes long-term liver inflammation that indicates the advanced
stages of liver diseases, including fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), which
finally leads to the death of infected patients. High-throughput T cell receptor sequencing reveals
distinct repertoires between tumor and adjacent non-tumor tissues in HBV-associated HCC.
Previously resolved HBV infection is defined by the presence of both anti-HBs and anti-HBc,
whereas the presence of anti-HBs alone indicates immunity to HBV infection following vaccination.
Fatigue can develop at anytime and there is no relationship between viral RNA and its genotype as
well as histology of the liver in the development of fatigue ( 110 ). In chronic hepatitis B virus
(HBV) carriers, elevated serum HBV DNA levels have been. Targeting the immunosuppressive
patients, host-signal targeting approach and including the antitumor responses by cell dysfunction
will also be highly fruitful to combat the HCV-induced HCC. That is, the patient will become e
antigen positive again, and start replicating. Evidence suggested that different inflammatory
cytokines such as IL-1, IL-23, IL-6, and lymphotoxins (LT) were involved in the development and
progress of liver inflammation and HCC ( 32 ). It's also our only finite therapy, which is important
for some patients. HBV infection can be broadly categorized as acute (primary) and chronic
(persistent) infection, which may be asymptomatic or mild (without significant liver injury) to severe
or fulminant. High hepatitis b viral load predicts recurrence of small hepatocellular carcinoma after
curative resection. The present study focused on the compilation and review of (30) papers on the
prevalence of HBV infection by Iraqi researchers in different areas of Iraq. Sharifi-Rad M, Anil
Kumar NV, Zucca P, Varoni EM, Dini L, Panzarini E, et al.
WHO recommended joint immunoprophylaxis starting from the newborn, multiple. I would like to
thank my colleagues, Nancy Reau and. Also known as occult HBV infection, patients in this phase
have normal ALT values and usually undetectable serum HBV DNA. This activity led to the strong
establishment of a chronic infection. But still, the mechanism needs to be further explored ( 7 ).
Viral hepatitis and Parkinson disease: A national record-linkage study. The lymphoid system in
hepatitis c virus infection: Autoimmunity, mixed cryoglobulinemia, and overt b-cell malignancy.
These markers should be monitored at least annually, and more frequently for patients receiving
antiviral treatment, following such treatment, and not yet meeting the criteria for such treatment. The
total global infection of HCV is estimated at 177.5 million infected adults, and it is expected that 1.6
million new infections occur every year ( 2, 3 ). Sustained response of hepatitis B e antigen-negative
patients 3 years after treatment. The HCC cells secrete the factors responsible for the activation of
endothelial cells by VEGF and FGF. Article types Author guidelines Editor guidelines Publishing
fees Submission checklist Contact editorial office Frontiers in Immunology. Similarly, Figure 2
showed the selection procedure of studies on the HBV load and HCC recurrence. One potential
explanation for this null association might be related to limited sample size in higher category of
HBV DNA. Third, dynamic HBV replication may trigger chronic hepatopathy with gangrenous
inflammation. The most common symptoms include fever, fatigue, decreased appetite, nausea,
vomiting, abdominal pain, dark urine, pale feces, joint pain, and jaundice. These markers can
accurately measure the virus-induced cellular stress that leads to HCC. The world is of a high
prevalence of HBsAg, especially eastern Asian. So, I would say that resistance is not as big a worry,
but the corollary is that this is only true if the patient is compliant with the medication and you have
suppressed virus to undetectable levels. Scudder, DNP, NP, has disclosed no relevant financial
relationships. Regulatory T cells in chronic hepatitis B patients affect the immunopathogenesis of
hepatocellular carcinoma by suppressing the anti-tumour immune responses. TLR response to hcv
infection Toll-like receptors (TLRs) are the most important molecules that produce cytokines and
signaling pathways that provide a link between innate and acquired immunity. When we conducted
stratified analysis according to median duration of follow-up, study style and primary treatment
method, the contribution of HBV load to HCC recurrence for all subgroups was similar to that for
the overall analysis. Additionally, there are many etiological factors, including genetic and
environmental conditions, that trigger the process of neurological disorders ( 137 ). The dose-
response meta-analysis was precisely performed to calculate the summary relative risks (RRs) by
quantizing the association between HBV load and risk of HCC. Many mechanisms that have been
proposed for the failure of the host response to viral clearances. Micro32. A 54-year-old man
presents to the clinic with scleral icterus. Predictors of mental and physical health in non-cirrhotic
patients with viral hepatitis: A case control study. Peripheral and central nervous system involvement
in essential mixed cryoglobulinemia: A case report. During follow-up, decompensation of disease
occurred in 46 subjects: 8 developed HCC, 36 developed ascites, and 2 developed jaundice.
Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2018 Apr. Patterns of HBV
markers seen during acute and chronic HBV infection are shown in Figure 2. Recently, the genetic
compartmentalization of HCV in the CSF of HCV-infected patients with cognitively impaired
symptoms has been demonstrated by deep sequencing techniques ( 87 ). Additionally, some
lncRNAs (LINC01419, BC014579, AK021443, RP11-401P9.4, RP11-304 L19.5, CTB-167B5.2,
and AF070632) are also known to be differentially expressed in HCC tissues and they are being
used as biomarkers for HCC detection ( 55 ). In addition, engineering HBV-specific T cells based on
HBV transcriptomes of HCC cells was thought to be useful for personalized immunotherapy ( 91 ).
Thus, the PD-L1 expression related score model has the potential to be a reliable predictor of
response to anti-PD-1 therapy. Younossi Z, Park H, Henry L, Adeyemi A, Stepanova M. Hepatitis c
virus syndrome: A constellation of organ- and non-organ specific autoimmune disorders, b-cell non-
hodgkin's lymphoma, and cancer. Prognostic determinants for chronic hepatitis B in Asians:
therapeutic implications. Gut. Sliter DA, Martinez J, Hao L, Chen X, Sun N, Fischer TD, et al.
Hepatitis c virus-related central and peripheral nervous system disorders. In addition, it increases
lipid peroxidation and disrupts mitochondrial function by altering the double-layer lipoprotein of the
mitochondrial membrane ( 22, 23 ). Hepatitis c virus and hepatocellular carcinoma: when the host
loses its grip. Eric K.H. Chan1, Natalie V.J. Aldhouse2, Helen Kitchen2, Hannah C. Weissenborn K,
Ennen JC, Bokemeyer M, Ahl B, Wurster U, Tillmann H, et al. HCV infection may be improved
using an appropriate diagnosis and direct antiviral therapy for sustained virological response. In the
innate immune response to chronic hepatitis C infection of the host, viral loss at the NK cell surface is
associated with HCV persistence. There is an urgent need to know and understand more about the
complex microenvironment of the liver and viral infection as well as cirrhosis. These are known as
RASAL1, EGLN3, CSMD1, CDKN2A, BCORL1, SFRP1, ZNF382, RUNX3, LOX, RB1, and
P73. Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma. Surface antigen: The
outer coating of the virus is made up of the surface antigen or. A probability value for nonlinearity
was calculated by testing the null hypothesis that the coefficient of the second spline was equal to
zero. Zhou P, Xia J, Zhou Y-J, Wan J, Li L, Bao J, et al. RR and the corresponding 95% CI were
calculated to estimate the effect of HBV DNA level on HCC. Feasibility and safety of nivolumab in
advanced hepatocellular carcinoma: real-life experience from three German centers. Deep sequencing
of hepatitis c virus reveals genetic compartmentalization in cerebrospinal fluid from cognitively
impaired patients. Similar results were found in HCV-infected patients, none of whom achieved a
sustained virological response such as a reduction in HCV RNA levels lasting for 24 weeks ( 57 ). Dr.
Reau does not intend to discuss investigational drugs, mechanical devices, biologics, or diagnostics
not approved by the FDA for use in the United States. Ogdie A, Pang WG, Forde KA, Samir BD,
Mulugeta L, Chang K-M, et al. Seventeen patients (36.2%) died or underwent liver transplantation.
Approximately 90% of patients with this syndrome are women of mid or older age. This website
also contains material copyrighted by 3rd parties. Currently, many targets can be used for developing
serum-based novel biomarkers. Anti-PD-1 antibody SHR-1210 combined with apatinib for advanced
hepatocellular carcinoma, gastric, or esophagogastric junction cancer: an open-label, dose escalation
and expansion study. Work-role of Radiation Therapists in the Consequences of Adaptive
Radiotherap. In HBV-related HCC, data from high-throughput sequencing (HTS) technology
showed that TCR diversity in tumors was higher than in adjacent non-tumor tissues. Article types
Author guidelines Editor guidelines Publishing fees Submission checklist Contact editorial office.
However, the relationship between hepatic steatosis and the severity of fibrosis is inconclusive, and
fibrosis is thought to result from metabolic syndrome (obesity, dyslipidemia, hypertension, and
insulin resistance) instead. Abhinav S Bursitis is inflammation or irritation of a bursa sac. During the
infection, HCV uses several mechanisms that lead to the development of HCC ( Table 1 ). There are
many CNS complications such as cerebrovascular, neuropathology, encephalic inflammation,
autoimmune, meningeal, and rheumatic disorders, which are known with the HCV infection ( 69 ).
The symptoms of cryoglobulinemia include leukocytoclastic vasculitis, transmural fibrinoid necrosis,
peripheral neuropathy, and thrombotic lumen occlusion ( 94 ). HCV-induced fibrosis has been
observed more in HIV-coinfected patients than in mono-infected patients ( 52, 53 ). Lncrnas in hcv
infection and hcv-related liver disease. Hepatocarcinogenesis in hepatitis c: Hcv shrewdly
exacerbates oxidative stress by modulating both production and scavenging of reactive oxygen
species. Further therapeutic goals are to prevent disease transmission to offspring, HBV reactivation,
HBV-associated extrahepatic manifestations, and to achieve regression of fibrosis and cirrhosis.
Interestingly, these enrolled HCC patients were all HBV-infected and with heavy tumor burdens,
suggesting that the combination therapy likely had greater efficacy than single-agent immunotherapy
( Table 1 ). In the host adaptive immune response to acute HCV infection, the activation of response
is observed several weeks after the HCV infection. Motor-axonal polyneuropathy associated with
hepatitis c virus. Phase III study of pembrolizumab (pembro) versus best supportive care (BSC) for
second-line therapy in advanced hepatocellular carcinoma (aHCC): KEYNOTE-240 Asian subgroup.
Additionally, chronic HCV infection also leads to imbalances in metabolic activities, especially the
glucose homeostasis and lipid metabolism, as well as the induction of type II diabetes in the infected
patients ( 69, 98 ). These are known as RASAL1, EGLN3, CSMD1, CDKN2A, BCORL1, SFRP1,
ZNF382, RUNX3, LOX, RB1, and P73. The expression of CD-81, SR-BI, and claudin 1 on
epithelial and endothelial cells takes place, but the entry of the virus can be prevented by developing
antibodies derived from cerebral endothelium, and in this way, they can be used as entry targets for
the virus in the brain ( 81, 82 ). Authier FJ, Bassez G, Payan C, Guillevin L, Pawlotsky JM, Degos
JD, et al. The regulation of histone acetylation is controlled by histone acetyltransferases (HATs) and
histone deacetylases (HDACs) that lead to HCC development in HCV-infected patients. New
developments in hbv molecular diagnostics and quantitative serology. The viral RNA was identified
in post-mortem brain tissue. Among those with cirrhosis, the five-year cumulative risk of hepatic
decompensation is 20%, and the annual risk of HCC ranges from 2% to 5%. 8 The factors affecting
the rate of HBV disease progression can be broadly categorized as host-related, viral-related, and
external. Excellent response to anti-PD-1 therapy in a patient with hepatocellular carcinoma: case
report and review of literature. The AFP is present in three different forms, known as AFP-L1, AFP-
L2, and AFP-L3.