Hepatitis B
Rehan Haider1, Asghar Mehdi2, Geetha Kumari Das3,
Zameer Ahmed4, Sambreen Zameer5
University Karachi,
Pakistan1,2,4,5
University Rajasthan,
India3
Email: rehan_haider64@yahoo.com, drasgharmedhi@gmail.com, dasgeetha342@gmail.com,
ahmed_dr2003@yahoo.com, sambreenzameer@yahoo.com
KEYWORDS |
ABSTRACT |
hepatitis B virus, chronic hepatitis B, liver
cirrhosis, hepatocellular carcinoma, transmission, vaccination. |
Hepatitis B is a viral infection caused by the Hepatitis B virus
(HBV), primarily affecting the liver and leading to both acute and chronic
disease. With over 250 million individuals suffering from chronic Hepatitis
B, it poses a significant global health challenge, being a leading cause of
liver cirrhosis, liver failure, and hepatocellular carcinoma. This study aims
to elucidate the transmission pathways, treatment options, and necessary
public health strategies for Hepatitis B. We analyze the modes of
transmission, which include contact with infectious body fluids—primarily
through perinatal transmission, unprotected sexual contact, and sharing
contaminated needles. Despite the availability of an effective vaccine since
the 1980s, Hepatitis B remains endemic in many parts of Asia and Africa due
to limited immunization coverage. The pathogenesis of HBV involves complex
interactions between the virus and the host immune system, potentially
leading to liver inflammation and fibrosis. Clinical presentations vary
widely, ranging from asymptomatic infections to severe liver disease. Current
treatment options for chronic Hepatitis B include antiviral medications such
as tenofovir and entecavir, which suppress viral replication but do not cure
the infection. Recent advancements in therapeutic strategies, including novel
antivirals and immune modulators, show promise for more effective management
and potential cures in the future. Comprehensive public health
strategies—such as vaccination, screening, and education—are crucial for
controlling the spread of HBV and reducing the global burden of Hepatitis
B-related complications. |
DOI:
10.58860/ijsh.v3i9.234 |
|
Corresponding
Author: Rehan Haider*
Email: rehan_haider64@yahoo.com
INTRODUCTION
Approximately
one-third of the global population shows serological evidence of past or
current Hepatitis B Virus (HBV) infection (Cusi et al., 2022). Despite the
availability of HBV vaccines, the worldwide prevalence of chronic HBV infection
is estimated to be 3.7%. According to the World Health Organization (WHO), in
2015, 257 million people were living with chronic HBV infection (defined as
HBsAg positive), leading to approximately 887,000 deaths, primarily due to
cirrhosis and hepatocellular carcinoma. Since the discovery of HBV by Blumberg
in 1965, significant advancements have been made, including the introduction of
effective vaccines in the 1980s and the development of potent antiviral drugs
two decades later (Locarnini, Hatzakis, Chen, & Lok, 2015). However, the
global burden of chronic HBV remains significant, and complete eradication of
chronic HBV remains elusive. There is a considerable variation in HBV
prevalence across different regions, ranging from 0.1% to 20%. Low-prevalence
regions (<2%), such as Western Europe, North America, Canada, Australia, and
New Zealand, have a lifetime infection risk of less than 20%. Intermediate
prevalence (2% to 7%) regions, including Mediterranean countries, Japan,
Central Asia, the Middle East, and Latin and South America, account for
approximately 43% of the world's population, with a lifetime infection risk of
20-60%. High-prevalence regions (≥8%), such as Southeast Asia, China, and
sub-Saharan Africa, have a lifetime infection risk exceeding 60%. The variable prevalence
rates are associated with differences in age at infection and the corresponding
risk of chronicity (Grados et al., 2022). The progression rate from acute to
chronic HBV infection decreases with age, with approximately 90% of perinatal
infections progressing to chronicity, compared to 5% or less for adult
infections.
The ways in
which HBV is broadcast have changed considerably across various terrestrial
domains
Sexual
broadcast of HBV in unvaccinated things generally happens between heterosexual
men and women who have diversified intercourse participants or trade sexuality
labourers, and among fathers, the one has sex with different partners
accompanying guys (MSM). In reduced-prevalence fields, intercourse broadcast is
the main route of HBV broadcast
Percutaneous
broadcast is a direct fashion of HBV broadcast, accompanying a risk of up to
30% in things outside post-uncovering precaution (PEP) or able immunization.
The most meaningful percutaneous transmission route is giving teases and
syringes between communities where one introduces drugs (PWID), accounting for
about 15% of recently stated HBV contaminations in suppressed dominance domains
in Europe and the United States. Sharing razors or toothbrushes is another
potential route of percutaneous transmission, even though the certain risk is
mysterious. Additionally, practices inthewaythat acupuncture, tapabeat, and
bulk fierce have been guiding HBV broadcast. Public health instruction and the
use of sole-use teases or supplies are essential preventive measures
Perinatal
broadcast is the bigger route of HBV broadcast in many parts of the world and a
meaningful cause in asserting the repository of contamination, exceptionally in
high-predominance districts. In the omission of precaution, never-ending HBV
contamination will develop in 80% to 90% of babies innate to inventors the one are helpful for HBV e antigen (HBeAg)
All girls
should be tested for HBsAg at the first fetal visit/first trimester and this
can recur later in gestation if appropriate
Anti-HBV
situation of the parent with nucleoside analogues concedes the possibility of
being deliberate, especially in founders with extreme HBV DNA levels. The use
of telbivudine, lamivudine, and tenofovir is expected safe in gestation with no
raised antagonistic maternal or before-birth consequence
Lamivudine
appears to be another cautious, low-cost, cost and evenly productive
alternative to prevent upright broadcast in well viraemic HBV-contaminated
pregnant girls. A meta-reasoning revealed that the use of any antiviral
medicine diminished mom-to-child transmission, as defined by HBV surface
irritant seropositivity (risk percentage = 0.3, 95% CI 0.2–0.4) or infant HBV
DNA seropositivity (risk percentage 5 0.3, 95% CI 0.2–0.5) at 6–12 months. As
said earlier, C-sections should not be acted on routinely. If the juvenile is
immunized, (s)he is granted permission to be breastfed
Horizontal broadcasts
contain household, intrafamilial, and offspring-to-youngster broadcasts via
minor breaks in the skin or slimy membranes. At least 50% of contaminations in
youngsters cannot be justified by mom-to-infant broadcasts and, in many native
domains, before the debut of neonatal vaccination, the predominance sick in
minors 7 to 14 age of age. HBV remnants are viable outside the human physique
for an extended end and are spreading in the surroundings for at least 7 days
Blood backers
are usually secluded for HBV surface antigen (HBsAg). Therefore, the occurrence
of transference-connected HBV has decreased considerably. The risk of taking
post-transference HBV depends on determinants like predominance and benefactor
testing game plans. In reduced predominance regions, it was supposed to be
individual to four per heap ancestry parts transfused
There are
various strategies for benefactor hide. Most nations use HBsAg to hide donors.
Others, containing the United States, use two together HBsAg and
antagonistic-HBc. Routine protection of antagonistic-HBc remains questionable,
as the precision is depressed and sufferers accompanying cleared hepatitis
should be forbade. Some nations, for example, the USA, Germany, Spain, and
Singapore, use tiny-pool deoxyribonucleic acid testing for HBV DNA hide.
Through this experiment, the risk of HBV broadcast through transfusion was
reduced to 1 in 1 million
Nosocomial
contamination can occur from patient to patient, from patient to health
management trader, and with the order reversed. HBV is considered the ultimate
usually sent ancestry-borne bacterium in the healthcare background. Despite the
exercise of prevention plans (containing the use of not important needles and
supplies, sterilization of surgical mechanisms, and immunization of healthcare
workers), recorded cases of nosocomial contamination happen. However, the exact
risk of nosocomial contamination is unknown. The number of cases stated from
this route is inclined to be minimized as many infections may be asymptomatic,
and only a part of unprotected patients are remembered
for the experiment. The occurrence of HBV infection in health management labourers
is inferior in the accepted population on account of routine immunization
Healthcare
employees who are HBV-positive are not mainly forbidden from active. HBeAg
negative healthcare peasants are not considered expected spreading, when in
fact, HBeAg positive healthcare peasants endure wearing double protection and
do not perform certain endeavours, expected defined on an individual base.
However, cases of broadcast from HBsAg definite, HBeAg negative surgeons to
their cases have been stated
The risk of
transmission of HBV through a person who is an expert harm (when the patient is
HBeAg beneficial) is supposed with 1:3
Transmission
of HBV infection has existed since the later transplantation of extrahepatic
tools from HBsAg-positive patrons (for example, sort, cornea)
In case of
uncovering HBV in one of the lifestyles mentioned above, post-uncovering
precaution is urged for all non-immunized persons. An inactive-alive
immunization is urged. The first quantity of passive and live immunization
should be taken as early as possible. 12 hours after the uncovering is a
regularly thought-out new time point for active post-uncovering precautions.
One lot of HBV-immunoglobulin (HBIG) should be executed in the intervening time
if the beginning is famous to be HBsAg helpful. The added two doses of cure
concede the possibility of being administered afterwards between 4 and 12–24
weeks. Vaccinated things accompanying a recorded response do not need
post-uncovering precautions. Individuals who have had no post-immunization
testing concede the possibility of being proven for antagonistic-HBs titer as
early as possible. If this is not attainable, or the antagonistic-HBs titer is
lacking (<100 IU/L), they will require a second course of immunization.
Individuals the one are recorded non-responders will demand two doses of HBIG
given the individual temporal length of the event or entity's existence
The range of
dispassionate proofs of HBV contamination varies in two together severe and
incessant diseases. During the severe phase, exhibitions range from subclinical
or anicteric hepatitis to icteric hepatitis and, in a few cases, dangerous
hepatitis
After HBV
contamination, the process of early development ending ends from one to four months.
An earlier chapter can be performed before severe hepatitis develops. During
this end, an antitoxin syndrome-like disease may be cultivated. This condition
exhibits accompanying fever, skin rash, arthralgia, and arthritis. It will
mostly stop accompanying the attack of hepatitis. At least 70% of patients,
therefore, have subclinical or anicteric hepatitis, while an inferior 30% have
expandicteric hepatitis. The most important dispassionate symptoms of hepatitis
are right above one of four equal parts: discomfort, sickness in the stomach,
jaundice, and added unspecific constitutional manifestations. In case of
coinfection accompanying different hepatitis viruses or additional underlying
liver ailment, the dispassionate course can be more harsh.
Symptoms, including jaundice, mainly cease after up to three months, but few
patients experience extended fatigue even following position or time
normalization of antitoxin aminotransferase concentrations. During the severe
phase, alanine and aspartate aminotransferase levels (ALT and AST) can increase
to 1000–2000 IU/L. ALT is usually above AST. Bilirubin levels concede the
possibility be normal in a solid portion of victims. In cases where one
recovers, normalization of antitoxin aminotransferases ordinarily happens
within one to four months. Persistent height of antitoxin ALT for an additional
six months signifies progress to chronic hepatitis.
The rate of
progress from severe to incessant HBV is generally determined by the age at
contamination
The antiviral
situation of inmates accompanying acute HBV customarily is not urged. In men,
the likelihood of dangerous HBV is inferior by 1%, and the probability of
progress to chronic HBV is less than 5%. Therefore, the situation of severe HBV
is primarily auxiliary to the majority of cases. Antiviral situations
accompanying HBV polymerase inhibitors may be considered in certain subsets of
sufferers, such as subjects with harsh or extended courses of HBV, subjects
coinfected with additional hepatitis viruses or fundamental liver afflictions,
inmates with immunosuppression, or victims accompanying volatile liver
disappointment undergoing liver transplantation. In addition, patient contacts
should be proven for HBV and immunized if appropriate.
In
adult-captured infection, HBV chronicity is 5% or lower, as noticed formerly.
In perinatally collected contamination, it is estimated that it is expected to
be nearly 90%, and 20–50%, for contaminations between the age of the individual
and five age. Most subjects will not have a past of acute hepatitis. Most
sufferers accompanying incessant HBV (CHB) are clinically asymptomatic.
Some concede
the possibility have nonspecific manifestations to a degree of fatigue. In most
instances, important dispassionate symptoms will cultivate only if liver
affliction progresses to decompensated cirrhosis. In addition, extrahepatic
proofs can cause syndromes. Accordingly, a physical checkup will be the normal
private instance. In leading liver ailment, there can be dispassionate signs of
incessant liver affliction, including splenomegaly, larcenist blemish one is
born with, caput medusae, palmar erythema, testicular disintegration,
gynecomastia. Patients accompanying decompensated cirrhosis, jaundice, ascites,
minor oedema, and encephalopathy concede a possibility be present
The organic
course of CHB contamination is contingent upon the interplay of fervid copy and
the host's invulnerable reaction. Other factors that grant permission to
imitate the progress of HBV-related liver ailment involve neuter, alcohol
devouring, and contributing contamination with different hepatitis viruses
There are
various conventional patterns of CHB captured in adults or later childhood. First,
contamination accompanying a wildtype HBV variant: There is the classic
necroinflammatory state accompanying high HBV DNA, HBeAg helpful, extreme ALT
and alive liver disease. Second, infection accompanying a pre-core mutation has
become much more prevalent than wild-type bacterium in recent years. After
contamination with a pre-core mutation, HBeAg was negative despite a big HBV
DNA copy and exalted ALT. Third, in a low or non-replicative stage, place
antitoxin ALT is usual, HBeAg is negative, anti-HBe antibodies are consistently
present, and HBV DNA is depressed, a suggestion of correction detectable. This
rank is characterized by prejudiced invulnerable control of the HBV infection. In
perinatally captured never-ending HBV contamination
there are three various states: (i) an invulnerable resistance time, (ii) an
immune green light step, and (iii) a late non-replicative point.
The immune
fortitude state, which usually ends at 10 to 30 age,
is characterized by extreme levels of HBV replication, as exhibited by the
apiece closeness of HBeAg and high levels of HBV DNA in antitoxin. However, there
is no evidence of live liver ailment as seen by rational antitoxin ALT concentrations
and the slightest changes in liver biopsy. It is hoped that this lack of liver
ailment, regardless of high levels of HBV copy, is on account of invulnerable
tolerance to HBV
Very few
patients with never-ending HBV infection enhance HBsAg negative in the normal
course of contamination
There is a
roomy alternative in the dispassionate consequence and prognosis of incessant
HBV contamination. A recent dossier showed that in France about three of the
victims accompanying incessant HBV who advanced to a liver-connected snag had a
supplementary liver-related risk determinant. The risk of progress is expected to
be higher if invulnerable incitement happens. Moreover, all-cause mortality in
HBsAg was raised, and helpful cases were noticed
a) Chronic
hepatitis to cirrhosis – 10 to 20%
b) Compensated
cirrhosis to hepatic decompensation – 20 to 30%
c) Compensated
cirrhosis to hepatocellular carcinoma – 5 to 15%
Survival rates are:
a) Compensated
cirrhosis – 85% at 5 age
b) Decompensated
cirrhosis – 55 to 70% converging old age and 15 to 35% at 5 age
Survival is
usually poor in patients accompanying signs of solid zealous copy distinguished
from victims who are HBV DNA negative or who have very depressed HBV DNA
levels. During the unaffected course of never-ending contamination, the
presence of the precore stop codon and basic gist promoter modifications
introduces the seroconversion from HBeAg to an antagonistic-HBe eagerness and
leads to the making conscious or alert of the invulnerable reaction. However,
variants grant permission to arise and bring about HBeAg negative CHB
accompanying extreme viremia levels. The predominance of HBeAg negative CHB has
been growing over the last decades. Acute exacerbations followed by extremely
vigorous copy-raised ALT levels and histological venture are common features of
HBeAg negative CHB superior to cirrhosis and HCC much faster than in HBeAg
helpful CHB victims.
In the current
age, HBV DNA levels have been connected to disease progress and have dismissed
HBeAg zeal as a flag for ailment endeavour. This is real both for progress to
cirrhosis and the risk of HCC. Therefore, most situational directions are
established for HBV viremia. A moderate halt to identify patients with a
reduced distinguished to extreme risk of progress and clue for the antiviral
situation is 104 log copies/mL (equivalent to nearly 2 x 103 IU/mL)
Heavy
intoxicating use guides faster HBV progression to liver harm and an exalted
risk of cultivating cirrhosis and HCC
In patients
accompanying HBV/HCV coinfection, HCV mostly holds sway. This may bring about
lower levels of transaminases and HBV DNA. The rate of HBsAg seroconversion
even performs expected raised, as there is a famous system of mysterious HBV
infection (subjects accompanying negative HBsAg but perceptible antitoxin HBV
DNA) in patients accompanying incessant HCV. Despite lower aminotransferases
and HBV DNA levels, liver damage is poor in most cases. The risks of harsh
hepatitis and volatile hepatic breakdown seem expected to be inflated if two
contaminations together occur simultaneously, although either it is a severe
coinfection of HBV and HCV or acute HCV in incessant HBV.
A severe
HBV/HDV coinfection is expected to be more severe than a severe HBV
contamination unique. It is more likely to influence volatile hepatitis. If HDV
superinfection happens in victims with CHB, HDV ordinarily dominates, and HBV
copy is restrained. The severity of liver disease is bad and progress to
cirrhosis is increased.
The two bigger
extrahepatic problems of never-ending HBV are polyarteritis nodosa and renal
impairment on account of glomerular disease. They happen in up to 10% of
victims accompanying incessant HBV and are hoped to be interceded by flowing
invulnerable complexes
The
dispassionate proofs are analogous to those of victims with polyarteritis the
ones that are HBV negative. Permissions are granted for a few clinical benefits
of antiviral healing. Nephropathy/Glomerulonephritis HBV can encourage two
together blurry nephropathy and, less frequently, membranoproliferative
glomerulonephritis. Most cases happen in children. The dispassionate
authentication is proteinuria. In contrast to polyarteritis nodosa, there is no
meaningful benefit of the antiviral situation.
METHOD
Objective
To inspect the
predominance, risk determinants, and consequences associated with Hepatitis B
contamination.
Type of Study
A
cross-localized study (or disciple study, case-control study, contingent upon
the objective). Participants. Include the number and headcount of members
(e.g., age, grammatical rules applying to nouns that connote sex or
animateness, nationality) of the ones who were proven for Hepatitis B. Sampling
Technique. Describe by what parties were picked (e.g., random examination,
availability examining, layered inspecting). Clinical Data. Blood samples were
calm from colleagues for the Hepatitis B surface antigen (HBsAg) experiment and
liver function tests (ALT, AST). Questionnaires. Participants achieved an
inquiry concerning risk determinants (for example, history of ancestry
transference, venous dependence on illegal substances, intercourse past, and
immunization status).
Laboratory Methods
Describe the
distinguishing tests secondhand for Hepatitis B discovery (like ELISA, PCR). Detail
some genotyping or energetic load estimates performed.
Statistical Tools
Mention the
spreadsheet secondhand for reasoning (for instance, SPSS, R).
Statistical Methods
Describe the
mathematical tests secondhand (e.g., u.s. city-square test, logistic reversion,
Cox equivalent hazards model) to recognize important risk determinants and
effects.
RESULT AND DISCUSSION
Demographic Characteristics:
Provide a
detailed demographic profile of the shareholders, including age, gender,
ethnicity, and other relevant socio-economic factors. This should be broken
down into specific categories to understand how these characteristics may
influence or correlate with Hepatitis B prevalence.
Prevalence of Hepatitis B:
Report the
proportion of participants who tested positive for Hepatitis B (HBsAg+). When
appropriate, present these results in greater detail by breaking them into
subgroups such as age categories, gender, ethnicity, and identified risk
factors. Highlight trends and patterns within these subgroups to provide a
clearer picture of the distribution of Hepatitis B.
Risk Factor Analysis:
Thoroughly
discuss the key risk factors associated with Hepatitis B infection, including
behaviors such as needle sharing, having multiple sexual partners, and lack of
vaccination (Furino, 2019). Provide a detailed statistical analysis, including
odds ratios (OR) or relative risks (RR) with their 95% confidence intervals
(CI) for each identified risk factor. This in-depth analysis will help identify
which factors have the most significant impact on infection rates.
Outcomes:
Describe the
clinical outcomes observed in participants diagnosed with Hepatitis B, such as
progression to chronic hepatitis, liver cirrhosis, or hepatocellular carcinoma.
Include the frequency and severity of these outcomes, and consider how they
vary across different demographic and risk groups to provide a nuanced
understanding of the disease's impact.
Interpretation of Results:
Analyze the
significance of the prevalence rates identified in this study. Compare these
rates with those of different ethnic groups or general population statistics.
Discuss the implications of the identified risk factors, evaluating whether
they align with existing literature and known epidemiological data. Explore
possible explanations for any unexpected findings, considering factors such as
genetic predispositions, socio-economic status, or access to healthcare.
Comparison with Previous Studies:
Compare the
findings of this study with those of previous research on Hepatitis B
(Bainbridge, Ludeke, & Smillie, 2022). Discuss similarities and differences
in prevalence rates, risk factors, and outcomes. Highlight how this study adds
to the existing body of knowledge and where it diverges, offering possible
reasons for these differences.
Strengths and Limitations:
Strengths:
Discuss the strengths of the study, such as a large sample size, comprehensive
data collection methods, or robust statistical analysis. Highlight how these
strengths contribute to the reliability and generalizability of the findings.
Limitations:
Acknowledge
the study's limitations, such as potential selection bias, reliance on
self-reported data, or the cross-sectional nature of the study that may limit
causal inferences. Discuss how these limitations might affect the study's
conclusions and suggest areas for future research.
Implications for Public Health:
Discuss how the findings can inform
public health interventions, such as targeted vaccination programs, educational
campaigns, or harm reduction strategies. Explain how these interventions could
be tailored based on the identified risk factors and demographic trends to
maximize their effectiveness in reducing the burden of Hepatitis B.
CONCLUSION
Summarize the
main verdicts of the study, stressing the predominance, risk determinants, and
consequences associated with Hepatitis B. Suggest pieces of advice established
the study judgments, in the way that raised hide in the high-risk populace,
supporter immunization game plans, or further research into direct situation
alternatives. Outline potential areas for future research, to a degree,
lengthwise studies to path the creation of Hepatitis B or studies putting on
the influence of various treatment regimes. The completion of this research
project would not have been possible without the contributions and support of
many individuals and organizations. We are deeply grateful to all those who
played a role in the success of this project. We would also like to thank My
Mentor [. Naweed Imam Syed, Prof. Department of Cell Biology at the University
of Calgary, and Dr. Sadaf Ahmed, Psychophysiology Lab University of Karachi,
for their invaluable input and support throughout the research. Their insights
and expertise were instrumental in shaping the direction of this project's Declaration
of Interest.
I, at this
moment, declare that I have no pecuniary or other personal interest, direct or
indirect, in any matter that raises or may raise a conflict with my duties as a
manager of my office. Management Conflicts of Interest The authors declare that they have no
conflicts of interest. Financial support and sponsorship No Funding was
received to assist with the preparation of this manuscript
REFERENCES
Arora, A., Singh, S. P., Kumar, A., Saraswat, V. A.,
Aggarwal, R., Bangar, M., … Wadhawan, M. (2018). INASL Position Statements on
Prevention, Diagnosis and Management of Hepatitis B Virus Infection in India:
The Andaman Statements. Journal of Clinical and Experimental Hepatology,
8(1), 58–80. Retrieved from https://doi.org/10.1016/j.jceh.2017.12.001
Austin, H. (2022). An evaluation of hepatitis B virus in
England and the host-virus interplay as a key determinant of disease outcomes.
The University of Liverpool (United Kingdom).
Bainbridge, T. F., Ludeke, S. G., & Smillie, L. D.
(2022). Evaluating the Big Five as an organizing framework for commonly used
psychological trait scales. Journal of Personality and Social Psychology,
122(4), 749.
Bastug, A., & Bodur, H. (2019). Acute Hepatitis B. Viral
Hepatitis: Acute Hepatitis, 25–44.
Bogler, Y., Wong, R. J., & Gish, R. G. (2018).
Epidemiology and natural history of chronic hepatitis B virus infection. Hepatitis
B Virus and Liver Disease, 63–89.
Cusi, K., Isaacs, S., Barb, D., Basu, R., Caprio, S.,
Garvey, W. T., … Younossi, Z. (2022). American Association of Clinical
Endocrinology Clinical Practice Guideline for the Diagnosis and Management of
Nonalcoholic Fatty Liver Disease in Primary Care and Endocrinology Clinical
Settings. Endocrine Practice, 28(5), 528–562. Retrieved from
https://doi.org/10.1016/j.eprac.2022.03.010
Furino, A. (2019). Health policy and the Hispanic.
Routledge.
García, M. P. S., Rojas, R. N. C., Pedraza, C., & Cano,
J. F. (2019). Severe Mental Illness Program, impact and response of structured
interentions in a group of patients in Bogota, Colombia. In American
Psychiatric Association (APA) 172nd Annual Meeting.
Glebe, D., Goldmann, N., Lauber, C., & Seitz, S. (2021).
HBV evolution and genetic variability: Impact on prevention, treatment and
development of antivirals. Antiviral Research, 186, 104973. Retrieved
from https://doi.org/10.1016/j.antiviral.2020.104973
Golos, A. M., Guntuku, S.-C., & Buttenheim, A. M.
(2024). “Do not inject our babies”: a social listening analysis of public
opinion about authorizing pediatric COVID-19 vaccines. Health Affairs
Scholar, 2(7).
Grados, L., Pérot, M., Barbezier, N., Delayre-Orthez, C.,
Bach, V., Fumery, M., … Gay-Quéheillard, J. (2022). How advanced are we on the
consequences of oral exposure to food contaminants on the occurrence of
chronic non communicable diseases? Chemosphere, 303, 135260. Retrieved
from https://doi.org/10.1016/j.chemosphere.2022.135260
Guardiola Arévalo, A., Gómez Rodríguez, R., Romero
Gutiérrez, M., Gómez Moreno, A. Z., García Vela, A., Sánchez Simón, R., …
Andrés Esteban, E. M. (2017). Characteristics and course of chronic hepatitis
B e antigen-negative infection. Gastroenterología y Hepatología (English
Edition), 40(2), 59–69. Retrieved from
https://doi.org/10.1016/j.gastre.2016.11.009
Khan, M. F., Khan, M. I., & Kato, I. (2023). Structural
and functional variation of human oral microbiome in health and disease. In Microbiome
and the Eye (pp. 19–86). Elsevier. Retrieved from
https://doi.org/10.1016/B978-0-323-98338-9.00002-5
Khuroo, M. S., & Khuroo, M. S. (2016). Hepatitis E: an
emerging global disease–from discovery towards control and cure. Journal of
Viral Hepatitis, 23(2), 68–79.
Kochoumian, E., Moore, J., Mina, B., & Cahill, K.
(2020). Infections and Their Mimics in Returning Travelers in the Critical
Care Unit. In Infectious Diseases and Antimicrobial Stewardship in Critical
Care Medicine (pp. 93–108). CRC Press.
Lau, K. C. K. (2020). Persistent Hepatitis B Virus in
Hepatic and Extrahepatic Reservoirs in Hepatitis B Virus Related Oncogenesis.
Leoni, S., Casabianca, A., Biagioni, B., & Serio, I.
(2022). Viral hepatitis: Innovations and expectations. World Journal of
Gastroenterology, 28(5), 517.
Locarnini, S., Hatzakis, A., Chen, D.-S., & Lok, A.
(2015). Strategies to control hepatitis B: Public policy, epidemiology,
vaccine and drugs. Journal of Hepatology, 62(1), S76–S86. Retrieved
from https://doi.org/10.1016/j.jhep.2015.01.018
Louten, J. (2016). Virus transmission and epidemiology. Essential
Human Virology, 71.
Murray, K. (2020). Exploring life changes for patients
diagnosed with’Alcoholic Liver Disease’-A qualitative study in Husserl’s and
Merleau-Ponty’s thought.
Nkomo, P., Naicker, N., Mathee, A., Galpin, J., Richter, L.
M., & Norris, S. A. (2018). The association between environmental lead
exposure with aggressive behavior, and dimensionality of direct and indirect
aggression during mid-adolescence: Birth to Twenty Plus cohort. Science of
The Total Environment, 612, 472–479. Retrieved from
https://doi.org/10.1016/j.scitotenv.2017.08.138
Omonga, N. F. (2020). The synthesis, isolation and
evaluation of novel anticancer and antibacterial therapeutics derived from
natural products. University of Salford (United Kingdom).
Ou, Q., Mu, H., Zhou, C., Zheng, Z., & Geng, J. (2021).
Liver diseases. Clinical Molecular Diagnostics, 463–492.
Pankhurst, C. L., & Coulter, W. A. (2017). Basic
guide to infection prevention and control in dentistry. John Wiley &
Sons.
Peleg, N., Issachar, A., Sneh Arbib, O., Cohen-Naftaly, M.,
Braun, M., Leshno, M., … Shlomai, A. (2019). Liver steatosis is a strong
predictor of mortality and cancer in chronic hepatitis B regardless of viral
load. JHEP Reports, 1(1), 9–16. Retrieved from
https://doi.org/10.1016/j.jhepr.2019.02.002
Razonable, R. R. (2020). M. Veronica Dioverti1. Diagnostic
Microbiology of the Immunocompromised Host, 97.
Rodríguez, M., Buti, M., Esteban, R., Lens, S., Prieto, M.,
Suárez, E., & García-Samaniego, J. (2020). Consensus document of the
Spanish Association for Study of the Liver on the treatment of hepatitis B
virus infection (2020). Gastroenterología y Hepatología (English Edition),
43(9), 559–587. Retrieved from https://doi.org/10.1016/j.gastre.2020.03.008
Saeed, S. (2019). The Hepatitis C treatment revolution:
Are key HIV-Hepatitis C Co-infected populations being left behind? McGill
University (Canada).
Salman, K., Rashmi, Priti, S., Molly, M., Kumar, V. S.,
& Zeenat, S. (2015). Hepatitis B virus infection in pregnant women and
transmission to newborns. Asian Pacific Journal of Tropical Disease,
5(6), 421–429. Retrieved from https://doi.org/10.1016/S2222-1808(15)60809-X
Stockdale, A. J. (2020). Hepatitis B and C in Malawi:
Epidemiology, Disease Burden and Opportunities for a Public Health Treatment
Programme. The University of Liverpool (United Kingdom).
Townsend, S. A., & Newsome, P. N. (2016). Non-alcoholic
fatty liver disease in 2016. British Medical Bulletin, 119(1), 143.
Triveni, G. S., Aggarwal, R., & Dwivedi, P. (2020).
Approach Antenatal Woman Attending Pregnant to. Clinical Methods in
Obstetrics & Gynecology, 3.
Yi, P., Chen, R., Huang, Y., Zhou, R.-R., & Fan, X.-G.
(2016). Management of mother-to-child transmission of hepatitis B virus:
Propositions and challenges. Journal of Clinical Virology, 77, 32–39.
Retrieved from https://doi.org/10.1016/j.jcv.2016.02.003
Yousaf, M. (2022). C-section birth data classification using
ensemble modelling techniques and their performance analysis.
Zhang, L., Gui, X., Teter, C., Zhong, H., Pang, Z., Ding,
L., … Zhang, L. (2014). Effects of hepatitis B immunization on prevention of
mother-to-infant transmission of hepatitis B virus and on the immune response
of infants towards hepatitis B vaccine. Vaccine, 32(46), 6091–6097.
Retrieved from https://doi.org/10.1016/j.vaccine.2014.08.078
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