Sandbox/HIV

HIV co infections

Coinfection	Epidemeology	Clinical features	Diagnosis	Treatment	Prevention
Tuberculosis	Tuberculosis (TB) infection occurs when a susceptible person inhales droplet nuclei containing Mycobacterium tuberculosis organisms In individuals with latent TB Infection, the risk of reactivation with TB disease increases very soon after HIV infection Rates of TB in the United States are declining, with 3.6 new cases per 100,000 population reported in 2010 As with TB in the general U.S. population, HIV-related TB disease is increasingly seen in people born outside of the United States	Common clinical symptoms of TB disease include productive cough, fever, sweats, weight loss, and fatigue. Culture-positive TB disease can be sub-clinical or oligo-symptomatic. In HIV-infected individuals, the presentation of active TB disease is influenced by the degree of immunodeficiency. Extrapulmonary disease is more common in HIV-infected individuals than in those who are uninfected, regardless of CD4 cell counts, although clinical manifestations are not substantially different from those described in HIV-uninfected individuals. In patients with advanced HIV disease, the chest radiographic findings of pulmonary TB are markedly different than those in patients with less severe immunosuppression. Lower lobe, middle lobe, interstitial, and miliary infiltrates are common and cavitation is less common. Intrathoracic lymphadenopathy is common, with mediastinal involvement seen more often than hilar adenopathy. The greater the degree of immunodeficiency, the higher the likelihood of extrapulmonary TB, such as lymphadenitis; pleuritis; pericarditis; and meningitis, all with or without pulmonary involvement, and it is found in most TB patients with CD4 cell counts <200 cells/mm3	Testing for LTBI at the time of HIV diagnosis should be routine, regardless of an individual’s epidemiological risk of TB exposure. Individuals with negative diagnostic tests for LTBI who have advanced HIV infection (CD4 cell count <200 cells/mm3 ) and no indications for initiating empiric LTBI treatment should be retested for LTBI once they start ART and attain a CD4 count ≥200 cells/mm Patients with HIV infection who travel or work internationally in settings with a high prevalence of TB should be counseled about the risk of TB acquisition and the advisability of testing for LTBI upon return Screening for symptoms (asking for cough of any duration) coupled with chest radiography is recommended to exclude TB disease in a patient with a positive TST or IGRA.	HIV-infected individuals who test positive for LTBI but have no evidence of TB disease should receive LTBI treatment (AI). HIV-infected close contacts of anyone who has infectious TB also should receive prophylaxis, regardless of results of screening tests for LTBI Isoniazid administered for 9 months remains the preferred therapy, with proven efficacy, good tolerability. Isoniazid can potentiate the risk of peripheral neuropathy when used with some antiretroviral (ARV) drugs, most notably the dideoxynucleosides (didanosine, stavudine), which are seldom used in clinical practice in the United States. Isoniazid, when used with efavirenz- or nevirapine- based regimens, does not significantly increase risk of hepatitis—the most important adverse effect. 42,43	The risk of recurrent TB in patients with HIV co-infection appears to be somewhat higher than in those who are HIV-uninfected and receiving the same TB treatment regimen in the same setting. 152 In TB-endemic settings, much of the increased risk of recurrent TB appears to be due to the higher risk of re-infection with a new strain of M. tuberculosis, with subsequent rapid progression to TB disease.153,154
Hepatitis B	Hepatitis B virus (HBV) is the leading cause of chronic liver disease worldwide. 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. 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. Genotype A is most common among patients in North America and Western Europe.	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 (i.e., 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.	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 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 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.	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 .and emtricitabine, regardless of the level of HBV DNA (AIII). Such a regimen will reduce the likelihood of immune reconstitution inflammatory syndrome (IRIS) against HBV	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. 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 (BII).34,35 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
Hepatitis C	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.1 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.5,6 HCV is approximately 10 times more infectious than HIV through percutaneous blood exposures and has been shown to survive for weeks in syringes.7-9 Heterosexual transmission of HCV is uncommon but more likely in those whose partners are co-infected with HIV and HCV.13,1 Incidence of mother-to-child HCV transmission is increased when mothers are HIV-co-infected, reaching rates of 10% to 20%.28,29	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 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	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 Persons who test positive for HCV antibody should undergo confirmatory testing by using a sensitive quantitative assay to measure plasma HCV RNA level	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). 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 (AI) 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 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	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. Relatively high rates of viral clearance have beenobserved with HCV treatment during the acute phase of infection