HIV AIDS Coinfections: Difference between revisions
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*Globally and in North America, approximately 10% of HIV-infected patients have evidence of chronic HBV infection. | *Globally and in North America, approximately 10% of HIV-infected patients have evidence of chronic HBV infection. | ||
*In countries with a low prevalence of endemic chronic HBV infection, the virus is transmitted primarily through sexual contact and injection drug use, whereas perinatal and early childhood exposures are responsible for most HBV transmission in higher prevalence regions. | *In countries with a low prevalence of endemic chronic HBV infection, the virus is transmitted primarily through sexual contact and injection drug use, whereas perinatal and early childhood exposures are responsible for most HBV transmission in higher prevalence regions. | ||
*Genotype A is most common among patients in North America and Western Europe. | *Genotype A is most common among patients in North America and Western Europe. | ||
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*Acute infection may be asymptomatic. | *Acute infection may be asymptomatic. | ||
*Symptoms may include right upper quadrant [[abdominal pain]], [[nausea]], [[vomiting]], [[fever]], and [[arthralgias]] with or without [[jaundice]]. Most patients with chronic HBV infection are asymptomatic or have non-specific symptoms, such as [[fatigue,]] until they develop cirrhosis and signs of [[portal hypertension]] like [[ascites]], [[variceal bleeding]], [[coagulopathy]], [[jaundice]], or [[hepatic encephalopathy]]). | *Although the general modes of transmission are similar to HIV, HBV is transmitted more efficiently than HIV. | ||
*HBV has an average incubation period of 90 days (range 60–150 days) from exposure to onset of jaundice and 60 days (range 40–90 days) from exposure to onset of abnormal liver enzymes. Genotypes of HBV (A–H) have been identified with different geographic distributions.*Symptoms may include right upper quadrant [[abdominal pain]], [[nausea]], [[vomiting]], [[fever]], and [[arthralgias]] with or without [[jaundice]]. Most patients with chronic HBV infection are asymptomatic or have non-specific symptoms, such as [[fatigue,]] until they develop cirrhosis and signs of [[portal hypertension]] like [[ascites]], [[variceal bleeding]], [[coagulopathy]], [[jaundice]], or [[hepatic encephalopathy]]). | |||
*[[Hepatocellular carcinoma]] (HCC) is asymptomatic in its early stages and usually, but not always, occurs in the setting of [[hepatitis-B]] or [[hepatitis-C]] related cirrhosis. | *[[Hepatocellular carcinoma]] (HCC) is asymptomatic in its early stages and usually, but not always, occurs in the setting of [[hepatitis-B]] or [[hepatitis-C]] related cirrhosis. | ||
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*All HIV-infected patients should be tested for HBV infection. Initial testing should include serologic testing ,for surface antigen (HBsAg), hepatitis B core antibody (anti-HBc total), and hepatitis B surface antibody (anti-HBs). | *All HIV-infected patients should be tested for HBV infection. Initial testing should include serologic testing ,for surface antigen (HBsAg), hepatitis B core antibody (anti-HBc total), and hepatitis B surface antibody (anti-HBs). | ||
*Chronic HBV infection is defined as persistent HbsAg detected on 2 occasions at least 6 months apart. Patients with chronic HBV infection should be further tested for HBV e-antigen (HBeAg), antibody to HBeAg (anti-HBe), and HBV DNA | *Chronic [[HBV]] infection is defined as persistent HbsAg detected on 2 occasions at least 6 months apart. Patients with chronic HBV infection should be further tested for HBV e-antigen (HBeAg), antibody to HBeAg (anti-HBe), and HBV DNA | ||
*The inactive chronic hepatitis B state is characterized by a negative HBeAg, normal ALT levels, and an HBV DNA level < 2,000 international units/mL. | *The inactive chronic hepatitis B state is characterized by a negative HBeAg, normal ALT levels, and an HBV DNA level < 2,000 international units/mL. | ||
*Patients diagnosed with chronic HBV infection should have a complete blood count, ALT, aspartate aminotransferase (AST), albumin and bilirubin levels, and prothrombin time monitored at baseline and every 6 months thereafter to assess severity and progression of liver disease | *Patients diagnosed with chronic [[HBV infection]] should have a complete blood count, [[ALT]], [[aspartate aminotransferase]] (AST), [[albumin]] and [[bilirubin levels]], and [[prothrombin time]] monitored at baseline and every 6 months thereafter to assess severity and progression of [[liver]] disease. | ||
*Liver biopsy with histologic examination remains a valuable tool for characterizing the activity and severity of chronic hepatitis B and may provide important information in monitoring disease progression, guiding treatment, and excluding other diseases. | *[[Liver biopsy]] with histologic examination remains a valuable tool for characterizing the activity and severity of chronic [[hepatitis B]] and may provide important information in monitoring disease progression, guiding treatment, and excluding other diseases. | ||
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*The ultimate treatment goals in HIV/HBV co-infection are the same as for HBV monoinfection: to prevent , disease progression and to reduce HBV-related morbidity and mortality. Anti-HBV therapy is indicated for elevated ALT and elevated HBV DNA >2,000 international units/mL or significant fibrosis (AI) | *The ultimate treatment goals in HIV/HBV co-infection are the same as for [[HBV]] monoinfection: to prevent , disease progression and to reduce HBV-related morbidity and mortality. Anti-HBV therapy is indicated for elevated ALT and elevated HBV DNA >2,000 international units/mL or significant fibrosis (AI) | ||
*For HIV/HBV co-infected individuals, ART must include two drugs active against HBV, preferably tenofovir | *For HIV/HBV co-infected individuals,[[ART]] must include two drugs active against HBV, preferably [[tenofovir]] and [[emtricitabine]], regardless of the level of HBV DNA . Such a regimen will reduce the likelihood of [[immune reconstitution inflammatory syndrome]] (IRIS) against [[HBV]]. | ||
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*HBV is primarily transmitted by percutaneous or mucosal exposure to infectious blood or body fluids. Therefore, HIV-infected patients should be counseled about transmission risks for HBV and avoidance of behaviors associated with such transmission. Counseling should emphasize the transmission risks associated with sharing needles and syringes, tattooing or body-piercing, and sexual transmission. | *HBV is primarily transmitted by percutaneous or mucosal exposure to infectious blood or body fluids. Therefore, HIV-infected patients should be counseled about transmission risks for HBV and avoidance of behaviors associated with such [[transmission]]. Counseling should emphasize the transmission risks associated with sharing needles and syringes, tattooing or body-piercing, and sexual transmission. | ||
*All household members and sexual contacts of patients with HBV should be screened and all susceptible contacts should receive both hepatitis A and B vaccines regardless of whether they are HIV infected. | *All household members and sexual contacts of patients with HBV should be screened and all susceptible contacts should receive both [[hepatitis A]] and B vaccines regardless of whether they are HIV infected. | ||
*Hepatitis B immunization is the most effective way to prevent HBV infection and its consequences | *[[Hepatitis B]] immunization is the most effective way to prevent HBV infection and its consequences. | ||
*Most HIV-infected patients with isolated anti-HBc are HBV DNA negative and not immune to HBV infection. They should be vaccinated with a complete series of hepatitis B vaccine followed by anti-HBs testing | *Most HIV-infected patients with isolated anti-HBc are HBV DNA negative and not immune to HBV infection. They should be vaccinated with a complete series of [[hepatitis B]] vaccine followed by anti-HBs testing <ref name="pmid14615664">{{cite journal| author=Gandhi RT, Wurcel A, McGovern B, Lee H, Shopis J, Corcoran CP et al.| title=Low prevalence of ongoing hepatitis B viremia in HIV-positive individuals with isolated antibody to hepatitis B core antigen. | journal=J Acquir Immune Defic Syndr | year= 2003 | volume= 34 | issue= 4 | pages= 439-41 | pmid=14615664 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14615664 }} </ref><ref name="pmid17214053">{{cite journal| author=Jongjirawisan Y, Ungulkraiwit P, Sungkanuparph S| title=Isolated antibody to hepatitis B core antigen in HIV-1 infected patients and a pilot study of vaccination to determine the anamnestic response. | journal=J Med Assoc Thai | year= 2006 | volume= 89 | issue= 12 | pages= 2028-34 | pmid=17214053 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17214053 }} </ref> | ||
*Hepatitis A vaccination is recommended for all hepatitis A antibody-negative patients who have chronic liver disease, are men who have sex with men, or who are injection drug users | *[[Hepatitis A]] vaccination is recommended for all hepatitis A antibody-negative patients who have chronic liver disease, are men who have sex with men, or who are injection drug users | ||
*Patients with chronic hepatitis B disease should be advised to avoid alcohol consumption | *Patients with chronic [[hepatitis B]] disease should be advised to avoid alcohol consumption | ||
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| style="padding: 5px 5px; background: #F5F5F5;" |'''[[HIV coinfection with hepatitis c]]''' | | style="padding: 5px 5px; background: #F5F5F5;" |'''[[HIV coinfection with hepatitis c]]''' | ||
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*Hepatitis C virus (HCV) is a single-stranded RNA virus; the estimated worldwide prevalence of HCV infection is 2% to 3%, which translates to an estimated 170 million infected individuals of whom approximately 3.2 million live in the United States. | *[[Hepatitis C]] virus (HCV) is a single-stranded RNA virus; the estimated worldwide prevalence of [[HCV]] infection is 2% to 3%, which translates to an estimated 170 million infected individuals of whom approximately 3.2 million live in the United States.<ref name="pmid17552026">{{cite journal| author=Alter MJ| title=Epidemiology of hepatitis C virus infection. | journal=World J Gastroenterol | year= 2007 | volume= 13 | issue= 17 | pages= 2436-41 | pmid=17552026 | doi= | pmc=PMC4146761 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17552026 }} </ref> | ||
*Seven distinct HCV genotypes have been described.2. | *Seven distinct [[HCV]] genotypes have been described.2. | ||
*Approximately, 20% to 30% of HIV-infected patients in the United States are co-infected with HCV. | *Approximately, 20% to 30% of HIV-infected patients in the United States are co-infected with HCV.<ref name="pmid12095384">{{cite journal| author=Sulkowski MS, Moore RD, Mehta SH, Chaisson RE, Thomas DL| title=Hepatitis C and progression of HIV disease. | journal=JAMA | year= 2002 | volume= 288 | issue= 2 | pages= 199-206 | pmid=12095384 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12095384 }} </ref><ref name="pmid20441517">{{cite journal| author=Ciesek S, Friesland M, Steinmann J, Becker B, Wedemeyer H, Manns MP et al.| title=How stable is the hepatitis C virus (HCV)? Environmental stability of HCV and its susceptibility to chemical biocides. | journal=J Infect Dis | year= 2010 | volume= 201 | issue= 12 | pages= 1859-66 | pmid=20441517 | doi=10.1086/652803 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20441517 }} </ref> | ||
*HCV is approximately 10 times more infectious than HIV through percutaneous blood exposures and has been shown to survive for weeks in syringes.7- | *[[HCV]] is approximately 10 times more infectious than HIV through percutaneous [[blood]] exposures and has been shown to survive for weeks in syringes.<ref name="pmid20726768">{{cite journal| author=Paintsil E, He H, Peters C, Lindenbach BD, Heimer R| title=Survival of hepatitis C virus in syringes: implication for transmission among injection drug users. | journal=J Infect Dis | year= 2010 | volume= 202 | issue= 7 | pages= 984-90 | pmid=20726768 | doi=10.1086/656212 | pmc=PMC2932767 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20726768 }} </ref> | ||
*Heterosexual transmission of HCV is uncommon but more likely in those whose partners are co-infected with HIV and HCV. | *Heterosexual transmission of [[HCV]] is uncommon but more likely in those whose partners are co-infected with HIV and [[HCV]].<ref name="pmid1656825 .">{{cite journal| author=Eyster ME, Alter HJ, Aledort LM, Quan S, Hatzakis A, Goedert JJ| title=Heterosexual co-transmission of hepatitis C virus (HCV) and human immunodeficiency virus (HIV). | journal=Ann Intern Med | year= 1991 | volume= 115 | issue= 10 | pages= 764-8 | pmid=1656825 . | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1656825 }} </ref> | ||
*Incidence of mother-to-child HCV transmission is increased when mothers are HIV-co-infected, reaching rates of 10% to 20%. | *Incidence of mother-to-child HCV transmission is increased when mothers are HIV-co-infected, reaching rates of 10% to 20%.<ref name="pmid16267758">{{cite journal| author=Mast EE, Hwang LY, Seto DS, Nolte FS, Nainan OV, Wurtzel H et al.| title=Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. | journal=J Infect Dis | year= 2005 | volume= 192 | issue= 11 | pages= 1880-9 | pmid=16267758 | doi=10.1086/497701 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16267758 }} </ref><ref name="pmid16352363 .">{{cite journal| author=Alter MJ| title=Epidemiology of viral hepatitis and HIV co-infection. | journal=J Hepatol | year= 2006 | volume= 44 | issue= 1 Suppl | pages= S6-9 | pmid=16352363 . | doi=10.1016/j.jhep.2005.11.004 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16352363 }} </ref> | ||
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*Both acute and chronic HCV infections are usually minimally symptomatic or asymptomatic. | *Both acute and chronic [[HCV]] [[infections]] are usually minimally symptomatic or asymptomatic. | ||
*Fewer than 20% of patients with acute infection have characteristic symptoms, including low-grade fever, mild right upper quadrant pain, nausea, vomiting, anorexia, dark urine, and jaundice | *Fewer than 20% of patients with acute infection have characteristic symptoms, including low-grade fever, mild right upper quadrant [[pain]], [[nausea]], [[vomiting]], [[anorexia]], [[dark urine]], and [[jaundice]] | ||
*Cirrhosis develops in approximately 20% of patients with chronic HCV infection within 20 years after infection, although the risk for an individual is highly variable | *[[Cirrhosis]] develops in approximately 20% of patients with chronic [[HCV]] infection within 20 years after infection, although the risk for an individual is highly variable | ||
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*All HIV-infected patients should undergo routine HCV screening | *All HIV-infected patients should undergo routine [[HCV]] screening | ||
* Initial testing for HCV should be performed using the most sensitive immunoassays licensed for detection of antibody to HCV (anti-HCV) in blood | * Initial testing for [[HCV]] should be performed using the most sensitive immunoassays licensed for detection of antibody to [[HCV]] (anti-HCV) in [[blood]]. | ||
*Persons who test positive for HCV antibody should undergo confirmatory testing by using a sensitive quantitative assay to measure plasma HCV RNA level | *Persons who test positive for HCV antibody should undergo confirmatory testing by using a sensitive quantitative assay to measure plasma HCV [[RNA]] level | ||
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*The goal of HCV therapy is to achieve a sustained virologic response (SVR). SVR is defined as the absence of detectable viremia ≥6 months after discontinuation of HCV treatment. | *The goal of [[HCV]] therapy is to achieve a sustained virologic response (SVR). SVR is defined as the absence of detectable viremia ≥6 months after discontinuation of [[HCV]] treatment. | ||
*HCV treatment recommendations are genotype specific as HCV genotype is an important determinant of the likelihood of response to interferon (IFN)-based HCV treatment regimens (genotype 2 > 3 > 1 and 4). | *[[HCV]] treatment recommendations are genotype specific as [[HCV]] genotype is an important determinant of the likelihood of response to [[interferon]] (IFN)-based HCV treatment regimens (genotype 2 > 3 > 1 and 4). | ||
*Host genetic polymorphisms near the interleukin-28B gene (IL28B encoding an interferon lambda) are strongly linked to spontaneous clearance of acute HCV infection and to response to IFN-based therapy for chronic HCV infection | *Host genetic polymorphisms near the [[interleukin]]-28B gene (IL28B encoding an interferon lambda) are strongly linked to spontaneous clearance of acute [[HCV]] infection and to response to IFN-based therapy for chronic HCV [[infection]] | ||
*The combination of peginterferon alfa (PegIFN) plus ribavirin is the recommended backbone of therapy for HIV/HCV-co-infected patients regardless of HCV genotype | *The combination of [[peginterferon alfa]] (PegIFN) plus [[ribavirin]] is the recommended backbone of therapy for HIV/HCV-co-infected patients regardless of HCV genotype. | ||
* HCV-genotype-1-infected patients who are not co-infected with HIV, a HCV NS3/4A PI, either boceprevir or telaprevir, in combination with PegIFN/ribavirin is recommended on the basis of large clinical trials | * HCV-genotype-1-infected patients who are not co-infected with HIV, a HCV NS3/4A PI, either [[boceprevir]] or [[telaprevir]], in combination with PegIFN/[[ribavirin]] is recommended on the basis of large clinical trials | ||
*Two formulations of PegIFN are available (alfa-2a and alfa-2b) for weekly subcutaneous injection. These agents are used for all HCV genotypes | *Two formulations of PegIFN are available (alfa-2a and alfa-2b) for weekly subcutaneous injection. These agents are used for all [[HCV]] genotypes | ||
*Ribavirin is recommended for use with PegIFN for all HCV genotypes. | *[[Ribavirin]] is recommended for use with PegIFN for all HCV genotypes. | ||
*Telaprevir is approved for use in combination with PegIFN/ribavirin in HCV-genotype-1- monoinfected-patients. The approved regimen for HCV monoinfected patients is telaprevir 750 mg orally (with at least 20 grams of fat) every 7 to 9 hours plus PegIFN/ribavirin for the initial 12 weeks of treatment followed by the discontinuation of telaprevir and the continuation of PegIFN/ribavirin for an additional 12 or 36 weeks, according to the observed HCV response at the end of treatment week 4 (response guided therapy | *[[Telaprevir]] is approved for use in combination with PegIFN/[[ribavirin]] in HCV-genotype-1- monoinfected-patients. The approved regimen for [[HCV]] monoinfected patients is [[telaprevir]] 750 mg orally (with at least 20 grams of fat) every 7 to 9 hours plus PegIFN/[[ribavirin]] for the initial 12 weeks of treatment followed by the discontinuation of [[telaprevir]] and the continuation of PegIFN/[[ribavirin]] for an additional 12 or 36 weeks, according to the observed HCV response at the end of treatment week 4 (response guided therapy | ||
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*The primary route of HCV transmission is drug injection via a syringe or other injection paraphernalia (i.e., “cookers,” filters, or water) previously used by an infected person. HCV-seronegative injection drug users should be encouraged to stop using injection drugs by entering a substance abuse treatment program or, if they are unwilling or unable to stop, to reduce the risk of transmission by never sharing needles or injection equipment. | *The primary route of [[HCV]] transmission is drug injection via a syringe or other injection paraphernalia (i.e., “cookers,” filters, or water) previously used by an infected person. HCV-seronegative injection drug users should be encouraged to stop using injection drugs by entering a substance abuse treatment program or, if they are unwilling or unable to stop, to reduce the risk of transmission by never sharing needles or injection equipment. | ||
*There is no vaccine or recommended post-exposure prophylaxis to prevent HCV infection. Following acute HCV infection, chronic infection may be prevented within the first 6 to 12 months after infection through treatment with peginterferon with or without ribavirin. | *There is no vaccine or recommended post-exposure prophylaxis to prevent HCV infection. Following acute HCV infection, chronic infection may be prevented within the first 6 to 12 months after infection through treatment with peginterferon with or without [[ribavirin]]. | ||
*Relatively high rates of viral clearance have beenobserved with HCV treatment during the acute phase of infection | *Relatively high rates of viral clearance have beenobserved with HCV treatment during the acute phase of infection | ||
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Revision as of 14:15, 20 October 2014
AIDS Microchapters |
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HIV AIDS Coinfections On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [2]
Overview
HIV Coinfetions are the diseases that are most commonly occuring along with HIV infections and hence they must be screened for in a HIV infected individual. The most commonly found coinfections are tuberculosis, hepatitis B and hepatitis C.
HIV Coinfections
Coinfection | Epidemeology | Clinical features | Diagnosis | Treatment | Prevention |
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HIV coinfection with tuberculosis |
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HIV coinfection with hepatitis b |
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HIV coinfection with hepatitis c |
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References
- ↑ Cain KP, McCarthy KD, Heilig CM, Monkongdee P, Tasaneeyapan T, Kanara N; et al. (2010). "An algorithm for tuberculosis screening and diagnosis in people with HIV". N Engl J Med. 362 (8): 707–16. doi:10.1056/NEJMoa0907488. PMID . 20181972 . Check
|pmid=
value (help). - ↑ Batungwanayo J, Taelman H, Dhote R, Bogaerts J, Allen S, Van de Perre P (1992). "Pulmonary tuberculosis in Kigali, Rwanda. Impact of human immunodeficiency virus infection on clinical and radiographic presentation". Am Rev Respir Dis. 146 (1): 53–6. doi:10.1164/ajrccm/146.1.53. PMID 1626814.
- ↑ Jones BE, Young SM, Antoniskis D, Davidson PT, Kramer F, Barnes PF (1993). "Relationship of the manifestations of tuberculosis to CD4 cell counts in patients with human immunodeficiency virus infection". Am Rev Respir Dis. 148 (5): 1292–7. doi:10.1164/ajrccm/148.5.1292. PMID . 7902049 . Check
|pmid=
value (help). - ↑ Perlman DC, el-Sadr WM, Nelson ET, Matts JP, Telzak EE, Salomon N; et al. (1997). "Variation of chest radiographic patterns in pulmonary tuberculosis by degree of human immunodeficiency virus-related immunosuppression. The Terry Beirn Community Programs for Clinical Research on AIDS (CPCRA). The AIDS Clinical Trials Group (ACTG)". Clin Infect Dis. 25 (2): 242–6. PMID . 9332519 . Check
|pmid=
value (help). - ↑ Tedla Z, Nyirenda S, Peeler C, Agizew T, Sibanda T, Motsamai O; et al. (2010). "Isoniazid-associated hepatitis and antiretroviral drugs during tuberculosis prophylaxis in hiv-infected adults in Botswana". Am J Respir Crit Care Med. 182 (2): 278–85. doi:10.1164/rccm.200911-1783OC. PMID 20378730.
- ↑ Hoffmann CJ, Charalambous S, Thio CL, Martin DJ, Pemba L, Fielding KL; et al. (2007). "Hepatotoxicity in an African antiretroviral therapy cohort: the effect of tuberculosis and hepatitis B." AIDS. 21 (10): 1301–8. doi:10.1097/QAD.0b013e32814e6b08. PMID 17545706.
- ↑ Osato T (1988). "[Viral infections in medicine. 5. EB virus, cytomegalovirus, herpesvirus infections diseases]". Nihon Naika Gakkai Zasshi. 77 (9): 1355–7. PMID 2854545.
- ↑ Narayanan S, Swaminathan S, Supply P, Shanmugam S, Narendran G, Hari L; et al. (2010). "Impact of HIV infection on the recurrence of tuberculosis in South India". J Infect Dis. 201 (5): 691–703. doi:10.1086/650528. PMID 20121433.
- ↑ Gandhi RT, Wurcel A, McGovern B, Lee H, Shopis J, Corcoran CP; et al. (2003). "Low prevalence of ongoing hepatitis B viremia in HIV-positive individuals with isolated antibody to hepatitis B core antigen". J Acquir Immune Defic Syndr. 34 (4): 439–41. PMID 14615664.
- ↑ Jongjirawisan Y, Ungulkraiwit P, Sungkanuparph S (2006). "Isolated antibody to hepatitis B core antigen in HIV-1 infected patients and a pilot study of vaccination to determine the anamnestic response". J Med Assoc Thai. 89 (12): 2028–34. PMID 17214053.
- ↑ Alter MJ (2007). "Epidemiology of hepatitis C virus infection". World J Gastroenterol. 13 (17): 2436–41. PMC 4146761. PMID 17552026.
- ↑ Sulkowski MS, Moore RD, Mehta SH, Chaisson RE, Thomas DL (2002). "Hepatitis C and progression of HIV disease". JAMA. 288 (2): 199–206. PMID 12095384.
- ↑ Ciesek S, Friesland M, Steinmann J, Becker B, Wedemeyer H, Manns MP; et al. (2010). "How stable is the hepatitis C virus (HCV)? Environmental stability of HCV and its susceptibility to chemical biocides". J Infect Dis. 201 (12): 1859–66. doi:10.1086/652803. PMID 20441517.
- ↑ Paintsil E, He H, Peters C, Lindenbach BD, Heimer R (2010). "Survival of hepatitis C virus in syringes: implication for transmission among injection drug users". J Infect Dis. 202 (7): 984–90. doi:10.1086/656212. PMC 2932767. PMID 20726768.
- ↑ Eyster ME, Alter HJ, Aledort LM, Quan S, Hatzakis A, Goedert JJ (1991). "Heterosexual co-transmission of hepatitis C virus (HCV) and human immunodeficiency virus (HIV)". Ann Intern Med. 115 (10): 764–8. PMID . 1656825 . Check
|pmid=
value (help). - ↑ Mast EE, Hwang LY, Seto DS, Nolte FS, Nainan OV, Wurtzel H; et al. (2005). "Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy". J Infect Dis. 192 (11): 1880–9. doi:10.1086/497701. PMID 16267758.
- ↑ Alter MJ (2006). "Epidemiology of viral hepatitis and HIV co-infection". J Hepatol. 44 (1 Suppl): S6–9. doi:10.1016/j.jhep.2005.11.004. PMID . 16352363 . Check
|pmid=
value (help).
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