Aids And Hepatitis B Are Caused By Pathogens

Factors Associated With Hbv And Hcv Co

To determine the factor associated with hepatitis co-infection we have performed a bivariate logistic regression analysis. In this phase variables with gender , age in years , residence , cigarette smoker , alcohol user , no condom usage , sharing of sharp materials , abstinence , and wise use of HAART treatment showed an association with hepatitis co-infection.

Then, variables with a p-value of less than 0.2 were further analyzed with multivariate analysis regression. However, in multivariable analysis, only wise use of HAART was significantly associated with hepatitis co-infection .

Can Hbv Infection Be Prevented

Yes. The best way to prevent HBV is to get the hepatitis B vaccine.

CDC recommends that people with HIV and people who are at risk for HIV get the HBV vaccine . The housemates and sexual partners of people with HBV should get the HBV vaccine, too.

People, including people with HIV, can also take the following steps to reduce their risk of HBV infection:

• Use condoms during sex to reduce the risk of HBV infection and infection with other sexually transmitted diseases, such as gonorrhea and syphilis.
• Do not inject drugs. But if you do, do not share needles, syringes, or other drug injection equipment.
• Do not share toothbrushes, razors, or other personal items that may come in contact with another person’s blood.
• If you get a tattoo or body piercing, make sure the instruments used are sterile.

Transmission Hbv Hcv And Hiv In Healthcare Settings

HIV, HBV and HCV are spread by contact with the blood of an infected person. The spread of these viruses from one person to another in healthcare settings is rare, but can occur. This contact is primarily through contaminated needles, syringes, or other sharp instruments. Medical experts emphasize that the careful practice of infection control procedures, including standard precautions , protects patients as well as healthcare providers from possible transmission in medical and dental settings.

Cleaning and Disinfection

See table of approved disinfectants in the PDF link below.

What does OSHA currently accept as “appropriate” disinfectants to prevent the spread of HIV and HBV?*

It is important to emphasize the EPA-approved label section titled “SPECIAL INSTRUCTIONS FOR CLEANING AND DECONTAMINATION AGAINST HIV-1 AND HBV Of SURFACES\ OBJECTS SOILED WITH BLOOD\BODY FLUIDS.” On the labels that OSHA has seen, these instructions require:

*Source:

What is the best way to clean up a blood spill?

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Ncert Exemplar Solutions Class 9 Science Chapter 13 Free Pdf Download

NCERT Exemplar Solutions for Class 9 Science Chapter 13 Why Do We Fall Ill is a vital study material for the Class 9 students as it has good marks allotment in the examination. Many times questions from this chapter are directly asked in competitive examination. Students who are planning to take biology in their higher secondary school should study this NCERT Exemplar thoroughly in order to understand the topic with ease. The NCERT Exemplar Solutions for Class 9 Science Chapter 13 is prepared by the highly experienced faculty after conducting vast research on each concept. While solving the textbook questions, students can refer to these solutions to get an overall idea about the topics covered in this chapter.

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Answer is hugs

Explanation

AIDS is transmitted by the exchange of body fluids. When we hug each other there cannot be an exchange of any body fluid hence AIDS cannot be transmitted by hugs.

9. Making anti-viral drugs is more difficult than making anti-bacterial medicines because

Pathogenesis Of Liver Disease

It seems paradoxical that HBV-related liver disease, which is an immune-mediated process, is exacerbated by the immunodeficient state caused by HIV. There are several possible reasons for this paradoxical relationship. In HIV-infected persons, a rapidly progressive form of liver disease due to viral cytopathic effect rather than the immune response, which is known as fibrosing cholestatic hepatitis, has been described. Thus, it is plausible that HBV variants, which can be more common in HIV infection, may account for a proportion of the increased liver disease in HIV coinfection., In support of this hypothesis, Revill et al. described a novel deletion mutation in the precore/core region of the HBV genome and found it to be more common among HIV-HBV coinfected than HBV monoinfected individuals. Coinfected persons with this mutation had higher HBV DNA levels than those without the mutation. In HBV monoinfected patients, core deletion mutations have been associated with more aggressive liver disease thus, this novel deletion mutant may contribute to liver disease progression in the setting of HIV infection.

It has also been hypothesized that HIV modulation of the HBV-specific immune response can alter the hepatic cytokine environment and subsequently affect liver disease. However, this hypothesis has not been studied to date.

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Prevalence Of Hiv In The World

In 2015, the number of HIV-related deaths ranged from 930,000 to 1,300,000 worldwide . According to Global AIDS in 2016, approximately, 37 million people live with HIV and 21 million are under treatment.

The distribution of HIV infection is not equitable in the world, sub-Saharan Africa is the most affected region. In 2015, it alone counted 25,600,000 people living with HIV or nearly 70% of the worlds PLHIV. The overall prevalence in this part of the world is 5.0% , with 1,900,000 new infections per year.

Should People With Hiv Get Tested For Hbv

CDC recommends that all people with HIV get tested for HBV. Testing can detect HBV even when a person has no symptoms of the infection.

There are several HBV blood tests. Results of different tests show different things. For example, a positive hepatitis B surface antigen test result shows that a person has acute or chronic HBV and can spread the virus to others.

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The Seroprevalence Of Hbv And Hbv

In this current study, the overall seroprevalence of hepatitis virus infection among HIV-positive patients attending at UoG-SRH was 21% . Furthermore, among hepatitis co-infected patients, the prevalence of HBV was found to be 13.6% . Among HBV co-infected participants, 45.45% were males and 54.55% of them were females. Also, the highest 54.55% HBV co-infection was found in the age groups of < 35 years .

The seroprevalence of HCV in HIV-positive participants is 8.6% . Among those participants, HCV is more prevalent in males than in females . In addition, the highest HCV seropositivity was seen in participants who come from an urban area . Furthermore, co-infection of HBV plus HCV among HIV-infected study participants amounted to 1.23% .

From a total of 21% hepatitis-infected individuals, 1.23% of the study participants developed all three viral infections .

Integration Of Hepatitis B Virus Dna

It has been long recognized that most tumors in HBV associated HCC contain clonally integrated HBV DNA and microdeletions in the flanking cellular DNA which could deregulate cellular growth control mechanisms . Indeed, in HCCs developed in woodchucks infected with woodchuck hepatitis B virus , WHV DNA insertions predominantly occur in the N-myc2 oncogene which leads to N-myc2 activation . Recent studies of HBV insertions in HBV-related HCCs revealed that also HBV integration can occur in genes that target telomerase and mixed lineage leukemia encoding genes suggesting potentially common pathways in HBV-related carcinogenesis . HBV DNA integration has also been observed in patients with chronic hepatitis suggesting that integration is likely an early step in the process of hepatocarcinogenesis . However, HBV integration is not likely occur in resting hepatocytes. Thus, if integration of the HBV genome contributes to hepatocarcinogenesis, it is likely to be secondary to procarcinogenic events that trigger hepatocyte turnover as described below.

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Role Of Viral Proteins

In addition to integration, it is possible that certain HBV proteins may directly participate in HCC development. For example, the HBV X gene product has been shown to transactivate cellular genes associated with cellular growth control . The HBV X protein has also been shown to interact and interfere with numerous transcription factors , nuclear factor interleukin- 6 , early growth response-1 , Ets-1, octamer-binding protein , and retinoid x receptor ], tumor suppressor genes , and proteins involved in DNA repair functions has been shown to be expressed from integrated subviral DNA in HCC and exert transcriptional activator activity . Likewise, the HBV large envelope has been shown to be a transcriptional transactivator . Thus, these viral products, expressed from integrated viral DNA or replicating virus may contribute to hepatocarcinogenesis by their capacity to activate a variety of cellular promoters .

Disease And Substance Prevention

Substance abuse treatment and community outreach programs that prevent substance abuse and promote safer drug-using habits can be extremely effective in preventing the spread of HIV and other infectious diseases, especially among injection drug users.

With funding from NIDA, the National AIDS Demonstration and Research projects implemented community outreach programs to prevent the spread of HIV among IDUs in 68 cities across the United States. Prevention outreach efforts typically included short encounters between IDUs and outreach workers who provided education about HIV transmission, condoms and bleach. An evaluation of 20 of the communities found that the percentage of IDUs at high risk of HIV infection fell from 62 percent to 31 percent six months after the initial contact with an outreach worker. Additionally, the number of IDUs who engaged in high-risk sexual behavior fell by nearly 50 percent.

Methadone maintenance programs reduced injection drug use from 81 percent to 29 percent after five years of treatment, according to UC Davis researchers.

Needle exchange programs also reduce the spread of disease among IDUs. The success of needle exchange programs is often measured by the number of IDUs who exchange used needles for sterile ones and the number of needles exchanged. Needle exchange programs generally lower disease risks among IDUs.

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Recommendations For Patients Requiring Hepatitis B Virus And Hiv Treatment

In patients with HIV and HBV coinfection, HBV infection should be treated only in conjunction with HIV infection. Treatment of HBV infection alone without addressing the HIV infection will lead to emergence of HIV strains that are resistant to nucleoside reverse-transcriptase inhibitors .

Only tenofovir is fully active for treatment in patients with known or suspected lamivudine-resistant HBV infection. Tenofovir is considered a first-line agent in patients with chronic HBV infection because the virologic efficacy is high and the risk for HBV resistance is low. Tenofovir is available in two preparations, tenofovir disoproxil fumarate and tenofovir alafenamide . TDF can lead to renal impairment and bone loss. The TAF formulation is associated with less renal toxicity and less effect on bone density.

In treatment-naive patients with HIV/HBV coinfection, a regimen containing TDF plus FTC or TDF plus 3TC should be used as the backbone of HIV therapy.

If TDF cannot be used, entecavir may be used to treat HBV infection however, owing to its weak activity against HIV, this is not considered an active component of the antiretroviral regimen. Lamivudine-resistant strains of HBV may rapidly develop resistance therefore, a higher dose is recommended with more frequent HBV viral load monitoring.

If the HIV therapy requires modification , the HBV-active antiretroviral must be continued and new antiretrovirals added to achieve HIV viral suppression.

Mechanisms Of Hepatocarcinogenesis During Hbv Infection

Multifactorial mechanisms contribute to the development of hepatocellular carcinoma in chronic HBV infection. Both viral and host factors including genetic alterations induced by viral DNA integration, expression of oncogenic viral proteins and chronic immune-mediated hepatitis have been implicated as contributing factors .

The chronic injury â HCC hypothesis. According to this hypothesis, a vigorous immune response to HBV leads to viral clearance while an absent immune response leads to the âhealthyâ carrier state, and an intermediate immune response produces chronic hepatitis. This indolent necroinflammatory liver disease is characterized by chronic liver cell necrosis which stimulates a sustained regenerative response. The inflammatory component includes activated macrophages that are a rich source of free radicals. The collaboration of these mitogenic and mutagenic stimuli has the potential to cause cellular and viral DNA damage, chromosomal abnormalities, genetic mutations, etc, that deregulate cellular growth control in a multistep process that eventually leads to hepatocellular carcinoma. Reprinted from Am J Pathol 2000, 156:1117â1132 with permission from the American Society for Investigative Pathology.

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What Is Hepatitis B

Hepatitis B is a liver infection caused by the hepatitis B virus . The abbreviation HBV can stand for either the virus or the infection it causes.

HBV can be a short-term or a long-term illness:

• Acute HBV occurs within 6 months after a person is exposed to HBV. In some people, acute HBV can lead to chronic HBV.
• Chronic HBV is a lifelong disease. Without treatment, chronic HBV can cause liver cancer or liver damage that leads to liver failure.

HBV is a contagious infection that can spread from person to person.

Data Entry And Analysis

First, the data were cleared by Epi-Info Version 7. Then, the data were extracted to the SPSS version 20 software for the data analysis. Then the data distribution was checked by the ShapiroWilk test. Then, descriptive statistics were summarized and presented in the form of figures and tables. The data were reported with mean and standard deviation for normally distributed data and median and interquartile range for skewed data. The association of the independent variable with the categorical outcome variable was measured by calculating the odds ratio with a 95% confidence interval using bivariate and multivariate logistic regression analysis. Variables having a p-value of less than 0.2 were selected for multivariate logistic regression analysis. To say a value was statistically significant the p-value must be < 0.05. Further, to show the strength of the association, the odds ratio with a 95% confidence interval was used.

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Genomic Structure And Organization

Morphologically, HIV is a single spherical particle with a diameter ranging from 90 to 120 nm. The virion has a spiky envelope and a dense nucleocapsid, sometimes trapezoidal or bar-shaped.

Structurally it is described as follows .

Figure 1.

HIV structure (from HIV genetic diversity and its consequences, .

The viral body comprises two identical RNA molecules three viral enzymes protease and integrase ] and three internal proteins .

The viral envelope, emanation of the cellular cytoplasmic membrane, carries two viral glycoproteins essential in the virus-host cell interaction. This is the gp41 and the gp120 .

HIV has gag, pol, and env as structural genes that encode internal proteins, viral enzymes, and envelope glycoproteins, respectively , and it has six regulatory genes: tat, rev, nef, alive, vpr, vpu , and vpx .

Figure 2.

Genomic organisation of HIV-1 and HIV-2 .

Initial Evaluation And Treatment Recommendations For Patients With Hepatitis C Virus/hiv Coinfections

Prior to initiating ART, screen patients with HIV infection for HCV using sensitive immunoassays licensed for the detection of antibody to HCV in blood to confirm the presence of chronic infection, persons who are HCV seropositive should be tested for HCV ribonucleic acid using a qualitative or quantitative assay.

Advise patients with HCV/HIV to avoid alcohol and receive HAV and HBV vaccines, if screened negative via serology.

Drug-induced liver injury following ART is more common in HIV/HCV coinfection eradication of HCV infection may decrease the likelihood of antiretrovirus-associated DILI.

It is important to monitor alanine aminotransferase and aspartate aminotransferase levels at 1 month and then every 3 months after the initiation of ART.

ART should be started in persons co-infected with HCV and HIV in accordance with the recommendations for initiating ART in treatment-naive patients. ART should be started at least 4-6 weeks before hepatitis C treatment is initiated.

The objective of HCV antiviral treatment is to cure the HCV infection, reflected by a sustained virologic response. Although patients with HIV and HCV coinfection traditionally had lower response rates to HCV treatment with older regimen of ribavirin and peginterferon compared to individuals without HIV infection, patients with coinfection appear to have comparable sustained virologic response rates with all oral, direct-acting antiviral combination therapy.

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Early Priming Of The Cd4 T Cell Response Is Required For Viral Clearance

Course of HBV infections, peripheral CD4+ T cell responses against HBV core protein, and intrahepatic CD8+ T cell responses in chimpanzees with or without CD4 immunodepletion as described in Asabe et al . Serum HBV DNA levels are shown as a black line and sALT as a yellow shaded area. Horizontal bars represent serum HBe and HBs antigen levels and the open horizontal bars represent the presence of anti-HBc, anti-HBe, and anti-HBs antibodies. The amount of each protein is reflected by the thickness of each bar as indicated in the legend. The numbers of CD4+ T cells per μL of whole blood were shown as closed squares . Arrows on the top panels represent injections of control antibody or anti-CD4 antibody . Peripheral CD4+ T cell IFNγ ELISPOT assays against HBV core protein and detection of intrahepatic HBV-specific CD8+ T cells were as described in except that freshly prepared cells were used instead of using cryopreserved cells. Fold induction of intrahepatic CD8 mRNA compared to two preinoculation time points is shown as a shaded red area . *: tested and negative. Reproduced/amended with permission from American Society for Microbiology from Journal of Virology, 2009, vol 83, pp. 9652â62, DOI: 10.1128/JVI.00867-09.