Aggressive Epstein‐Barr virus‐negative B‐cell post‐transplant lymphoproliferative disorder in a hepatitis C‐negative liver transplant recipient who received a hepatitis C‐positive graft: Implications for D+/R− hepatitis C virus seroconversion

Post‐transplant lymphoproliferative disorder (PTLD) is an uncommon, but well‐described complication after liver transplantation. Most recently, Hepatitis C virus (HCV) has been implicated in the development of PTLD. A HCV‐negative 62‐year‐old man with autoimmune hepatitis received a HCV nucleic acid amplification test‐positive liver graft from a 73‐year‐old brain‐dead donor (D+/R?). After his recovery from the operation, the patient was treated for HCV and achieved an undetectable viral load. He was readmitted 6 months after transplant with a spontaneous perisplenic hematoma, weight loss, failure to thrive, low‐grade fevers, and abnormal liver function tests. He had a rapid clinical deterioration and expired shortly after admission. His liver biopsy demonstrated EBV‐negative monomorphic B‐cell PTLD. Our case is the first to report an aggressive early‐onset EBV‐negative monomorphic B‐cell PTLD in a HCV D+/R? liver transplant. This case illustrates the paucity of knowledge on HCV seroconversion and its involvement in EBV‐negative monomorphic B‐cell PTLD development.     

The prevalence of hepatitis C virus (HCV) infection in HIV‐positive individuals in the UK – trends in HCV testing and the impact of HCV on HIV treatment outcomes

Summary. We examined the prevalence of hepatitis C virus (HCV) infection among HIV‐positive individuals in the UK, trends in HCV testing and the impact of HCV on HIV treatment outcomes. Trends over time in HCV prevalence were calculated using each patient’s most recent HCV status at the end of each calendar year. Logistic regression was used to identify factors associated with having a HCV antibody test, and Cox regression was used to determine whether HCV status was associated with the time to experiencing an immunological response to highly active antiretroviral treatment (HAART), time to virological response and viral rebound. Of the 31 765 HIV‐positive individuals seen for care between January 1996 and September 2007, 20 365 (64.1%) individuals were tested for HCV, and 1807 (8.9%) had detectable HCV antibody. The proportion of patients in follow‐up ever tested for HCV increased over time, from 782/8505 (9.2%) in 1996 to 14 280/17 872 (79.9%) in 2007. Nine thousand six hundred and sixty‐nine individuals started HAART for the first time in or after January 2000, of whom, 396 (4.1%) were HCV positive. Presence of HCV infection did not affect initial virological response, virological rebound or immunological response. The cumulative prevalence of HCV in the UK CHIC Study is 8.9%. Despite UK guidelines, over 20% of HIV‐positive individuals have not had their HCV status determined by 2007. HCV infection had no impact on HIV virological outcomes or immunological response to HIV treatment. The long‐term impact on morbidity and mortality remain to be determined.     

Change in transaminases in hepatitis C virus- and HIV-coinfected patients after highly active antiretroviral therapy: differences between complete and partial virologic responders?

Patients with HIV and hepatitis C virus (HCV) coinfection have more severe hepatitis-related disease than do patients with HCV infection alone. Highly active antiretroviral therapy (HAART) with protease inhibitor appears to restore pathogen-specific immune responses, especially in patients with persistent undetectable HIV viral load. To evaluate the potent impact of immune restoration induced by HAART on the course of HCV-related disease, HCV viremia and levels of transaminases were compared between two groups of patients: 10 HIV/HCV-coinfected patients with persistently undetectable HIV viremia (group A) and 12 HIV/HCV-coinfected patients with persistent detectable HIV viremia. No difference was detected in HCV viral load in either group. An increase in transaminases was found only in patients with persistent undetectable HIV viral load, which was correlated with the increase in CD8+ T cells. This may suggest that the restoration of CD8+ T cell cytotoxicity could lead to an enhancement of hepatitis C-related disease in HCV/HIV-coinfected patients receiving HAART.     

Successful treatment of donor‐derived hepatitis C viral infection in three transplant recipients from a donor at increased risk for bloodborne pathogens

We report here the successful treatment of hepatitis C virus (HCV) transmitted from a nucleic acid testing (NAT)‐negative donor to three HCV‐negative recipients—two renal transplants and one liver. Both renal recipients underwent standard deceased‐donor renal transplantation with immediate graft function. The liver recipient underwent standard orthotopic liver transplantation and recovered uneventfully. The donor was a 39‐year‐old woman with a terminal serum creatinine of 0.7 mg/dL. She was high risk for bloodborne pathogens, based upon a history of sexual contact with an HCV‐infected male partner. Recipient 1 was a 45‐year‐old man with a history of end‐stage renal disease from systemic lupus erythematosus. Recipient 2 was a 62‐year‐old woman with a history of end‐stage renal disease caused by hypertension and insulin‐dependent diabetes. Recipient 3 was a 42‐year‐old man with acute liver failure from acetaminophen ingestion. All recipients became HCV polymerase chain reaction positive on post‐transplant follow‐up. Both kidney recipients were treated with ledipasvir/sofosbuvir combination therapy for 12 weeks without side effects or rejection episodes. Recipient 3 was treated with ledipasvir/sofosbuvir in combination with ribavirin for 12 weeks without side effects. All patients achieved a sustained viral response at 12 weeks and are considered cured of HCV. The kidney recipients maintained good allograft function with a serum creatinine of 1.4 mg/dL and 1.0 mg/dL, respectively. Both renal recipients maintained normal liver function post treatment and did not develop any evidence of fibrosis. The liver recipient's liver function tests returned to normal without further incident. This case report provides evidence for the successful treatment of donor‐derived HCV in transplant recipients.     

Discordance in HIV-1 viral loads and antiretroviral drug concentrations comparing semen and blood plasma

Objectives

For individuals not on antiretroviral therapy, the risk of heterosexual transmission of HIV appears negligible when blood plasma (BP) viral loads are <1500 HIV‐1 RNA copies/mL. It is not clear whether this observation can be extrapolated to individuals on highly active antiretroviral therapy (HAART). Because of differential tissue penetration, antiretroviral drug concentrations may be sufficient to maintain an undetectable viral load in the BP yet not achieve adequate levels to suppress HIV in the genital tract. Therefore, we wanted to correlate HIV viral loads and drug concentrations in semen plasma (SP) and BP.

Methods

Thirty‐three men were included. All were on combination antiretroviral therapy with an undetectable BP viral load for at least 1 year. Blood and semen samples were collected within 2 h of each other and tested for HIV RNA by the NucliSens QT (bioMerieux, St Laurent, QC, Canada) method; drug concentrations were determined by liquid chromatography tandem mass spectrometry.

Results

Two of the 33 patients (6.1%) with BP viral loads below detection had time‐matched HIV viral loads in SP ≥700 copies/mL. Both patients were on efavirenz, the SP concentrations of which were ≤10% of the levels in BP and well below the minimal therapeutic drug monitoring target concentration required to suppress HIV.

Conclusions

Because, at least in part, of poor drug penetration into the genital tract, an undetectable HIV viral load in the BP does not guarantee an undetectable viral load in semen. In view of this, caution should be taken in concluding that patients on HAART with suppressed viraemia are sexually non‐infectious.     

European AIDS Clinical Society (EACS) guidelines for the clinical management and treatment of chronic hepatitis B and C coinfection in HIV-infected adults

OBJECTIVES: With the decline in HIV-associated morbidity and mortality following the introduction of highly active antiretroviral therapy (HAART), liver disease has emerged as a major cause of death in HIV/hepatitis B virus (HBV) and HIV/hepatitis C virus (HCV) coinfected persons. Therefore, screening for underlying viral hepatitis coinfection and the provision of management and treatment recommendations for patients with chronic viral hepatitis are of great importance in preventing, as far as possible, the development of liver disease. With the introduction of new agents for the treatment of hepatitis B and increased knowledge of how best to manage hepatitis C, an update of current guidelines for management of HBV and HCV coinfection with HIV is warranted. SUMMARY: Clearly, all HIV-infected patients should be screened for hepatitis A, B and C, taking into account shared pathways of transmission. Patients who are seronegative for hepatitis A and B should be considered for vaccination. In HIV-infected patients with chronic hepatitis B, the first important differentiation is whether HAART is required or not. In the setting of stable HIV infection, with no need for HAART, several treatment options are available, namely treatment with interferon, early initiation of HAART, or selective non-HIV active anti-HBV nucleoside therapy, with the aim of achieving undetectable HBV DNA levels. In most cases, undetectable HBV DNA can only be achieved with combination therapy. With regard to hepatitis C, individualized tailoring of the duration of HCV therapy is advisable, taking into account rapid or delayed virological response. In patients who do not achieve at least a 2 log drop in HCV RNA at week 12, treatment can be terminated because of the low probability of achieving sustained virological response. Overall, with the currently available treatment algorithms, HCV can be eradicated in over 50% of patients. Therefore, HCV therapy should be considered and discussed with the patient if an indication for HCV therapy (elevated liver enzymes, positive HCV RNA and >F1 fibrosis) is present. CONCLUSIONS: Management of underlying hepatitis B and/or C in patients with HIV infection is of great importance in preventing liver disease-associated morbidity and mortality.     

用高效抗逆转录病毒治疗HIV/HCV重叠感染33例

目的研究HIV/HCV重叠感染者用高效抗逆转录病毒治疗(HAART)的疗效和药物的副作用以及HIV和HCV的相互影响.方法治疗前后定期采集33例HIV/HCV重叠感染者的外周血,分离血桨和单个核细胞,检测病毒载量、T淋巴细胞亚群以及HCVRNA和肝脏纤维化指标.结果治疗后患者血浆中HIVRNA含量全部<50copies/ml,CD4不同程度增多.结论施多宁、拉米夫定和赛瑞特联合治疗HIV/HCV重叠感染者可有效抑制HIV-1的复制,并部分改善机体免疫功能.     

HCV recovery from peripheral blood mononuclear cell culture supernatants derived from HCV–HIV co-infected haemophilic patients with undetectable HCV viraemia

Hepatitis C viraemia, in 38 human immunodeficiency virus positive (HIV+)/hepatitis C virus positive (HCV+) patients, was determined in haemophilic patients during the 4 years since initiation of highly active antiretroviral therapy (HAART). Six of 38 patients had persistently HCV-negative viraemia for more than 2 years. No correlation between HCV-negative viraemia and CD4+ T-cell counts, HIV viral load, age, type or severity of haemophilia could be established. Reduced levels of HIV viral load and the immune reconstitution that follows the initiation of HAART were not enough to explain the disappearance of HCV from plasma. Individuals who cleared plasma HCV had significantly higher CD8+ T-cell counts (P=0.0013) (mean +/- SE: 1153 +/- 117.8 cells microL(-1)) than those with HCV-positive viraemia (819.1 +/- 40.72 cells microL(-1)). Because HCV could maintain a low replication level in peripheral blood mononuclear cells (PBMC), we cultured PBMC of five of six patients with undetectable HCV viraemia. We found four of five HCV RNA-positive cultures. The presence of HCV RNA in our cultures proved that these cells may be an important viral reservoir that could contribute to HCV recurrence in plasma even after long periods of negative viraemia. In summary, our results indicate that in spite of prolonged HCV-negative plasma viraemia, HCV patients that are co-infected with HIV may harbour replication-competent HCV in their PBMC. Therefore, true clearance of HCV infection is difficult to achieve in these patients.     

HIV–HCV co‐infected patients with low CD4+ cell nadirs are at risk for faster fibrosis progression and portal hypertension

Summary. Patients co‐infected with the human immunodeficiency virus (HIV) and the hepatitis C virus (HCV) are fraught with a rapid fibrosis progression rate and with complications of portal hypertension (PHT) We aimed to assess the influence of immune function [Centers of Disease Control and Prevention (CDC) stage] on development of PHT and disease progression in HIV–HCV co‐infection. Data of 74 interferon‐naïve HIV–HCV co‐infected patients undergoing liver biopsy, measurement of portal pressure and of liver stiffness and routine laboratory tests (including CD4+ cell count, HIV and HCV viral load) were analysed. Time of initial exposure (risk behaviour) was used to assess fibrosis progression. Fibrosis progression, time to cirrhosis and portal pressure were correlated with HIV status (CDC stage). HIV–HCV patients had rapid progression of fibrosis [0.201 ± 0.088 METAVIR fibrosis units/year (FU/y)] and accelerated time to cirrhosis (24 ± 13 years), high HCV viral loads (4.83 × 10⁶ IU/mL) and a mean HVPG at the upper limit of normal (5 mmHg). With moderate or severe immunodeficiency, fibrosis progression was even higher (CDC‐2 = 0.177 FU/y; CDC‐3 = 0.248 FU/y) compared with patients with higher CD4+ nadirs (CDC‐1 = 0.120 FU/y; P = 0.0001). An indirect correlation between CD4+ cell count and rate of fibrosis progression (R = ?0.6654; P < 0.001) could be demonstrated. Hepatic venous pressure gradient (HVPG) showed early elevation of portal pressure with median values of 4, 8 and 12 mmHg after 10, 15 and 20 years of HCV infection for CDC‐3 patients. Patients treated with highly active anti‐retroviral therapy (HAART) had similar rates of progression and portal pressure values than patients without HAART. Progression of HCV disease is accelerated in HIV–HCV co‐infection, being more pronounced in patients with low CD4+ cell count. A history of a CD4+ cell nadir <200/μL is a risk factor for rapid development of cirrhosis and PHT. Thus, HCV treatment should be considered early in patients with HIV–HCV co‐infection and largely preserved CD4+ cell counts.     

Pretreatment assessment and predictors of hepatitis C virus treatment in US veterans coinfected with HIV and hepatitis C virus

The US Department of Veterans Affairs (VA) cares for many human immunodeficiency virus/hepatitis C virus (HIV/HCV)-coinfected patients. VA treatment recommendations indicate that all HIV/HCV-coinfected patients undergo evaluation for HCV treatment and list pretreatment assessment tests. We compared clinical practice with these recommendations. We identified 377 HIV/HCV-coinfected veterans who began HCV therapy with pegylated interferon and ribavirin and 4135 HIV/HCV-coinfected veterans who did not but were in VA care at the same facilities during the same period. We compared laboratory and clinical characteristics of the two groups and estimated multivariate logistic regression models of receipt of HCV treatment. Overall, patients had high rates of receipt of tests necessary for HCV pretreatment assessment. Patients starting HCV treatment had higher alanine aminotransferase (ALT), lower creatinine, higher CD4 counts and lower HIV viral loads than patients not starting HCV treatment. In the multivariate model, positive predictors of starting HCV treatment included being non-Hispanic whites, having higher ALTs, lower creatinines, higher HCV viral loads, higher CD4 counts, undetectable HIV viral loads and receiving HIV antiretrovirals. A history of chronic mental illness and a history of hard drug use were negative predictors. Most HIV/HCV-coinfected patients received the necessary HCV pretreatment assessments, although rates of screening for hepatitis A and B immunity can be improved. Having well-controlled HIV disease is by far the most important modifiable factor affecting the receipt of HCV treatment. More research is needed to determine if the observed racial differences in starting HCV treatment reflect biological differences, provider behaviour or patient preference.     

Plasma Hepatitis C Virus Viral Load Among Hepatitis C Virus Mono-Infected and HCV/HIV Co-Infected Individuals in Yunnan Province,China

Background

Hepatitis C virus (HCV)/human immunodeficiency virus (HIV) co-infection has become a serious public health problem especially in high risk groups such as injection drug users in China. However, the impact of HIV infection and antiretroviral therapy (ART) on HCV viral load which is usually regarded as a predictor of liver disease progress had not been well studied in this country.

Objectives

To explore correlations of HIV co-infection and ART with plasma HCV load among HCV-infected patients in an ethnic minority area in Yunnan Province, China.

Patients and Methods

HCV/HIV co-infected patients and HCV mono-infected controls were examined and compared for plasma HCV RNA and related risk factors.

Results

A total of 145 HCV/HIV co-infected patients and 25 HCV mono-infected controls were studied. The majority of the participants were male, belonged to an ethnic minority and were younger than 45 years old. HCV viral suppression rate with undetectable plasma HCV viral load was 28.3% in the HCV/HIV co-infected patients, 36% among HCV mono-infected controls and 29.4% overall. ART-prescribed HCV/HIV co-infected patients had significantly higher HCV viral loads (IQR: (3.80-6.44)*log₁₀ copies ml-1) than those naïve to ART (IQR: (undetectable-6.41)*log₁₀ copies ml-1) and HCV mono-infected patients (IQR: (undetectable-5.44)*log₁₀ copies ml-1). Men, from the Dai minority and those with more than six years education, were also shown to have a higher plasma HCV viral load,according to multiple logistic regression analysis.

Conclusions

ART potentially increases the plasma HCV viral load among HCV/HIV coinfected patients in an ethnic minority area in China. Future large scale prospective cohort studies are needed to address the controversy associated between HIV co-infection and the natural history of HCV.     

Hepatitis C virus replication in Caucasian HIV controllers

Summary. Whether HIV controllers, patients who spontaneously control HIV viraemia, are able to control hepatitis C virus (HCV) infection, in terms of spontaneous clearance or lower HCV replication, is not well understood. To assess to what extent Caucasian HIV controllers are able to control HCV replication and potential associated factors, plasma HIV‐1 and HCV RNA levels, anti‐HCV antibodies, HCV genotype and human leucocyte antigens (HLA) typing were determined in samples from 75 HIV controllers (33 viraemic controllers, <1000 HIV‐1 RNA copies/mL, and 42 elite controllers, <40 HIV‐1 RNA copies/mL) and compared with 261 HIV‐infected noncontrollers. We did not find differences in the HCV spontaneous clearance rates between groups. However, we interestingly found a lower HCV viral load in HIV controllers, alongside a different distribution of HCV genotypes in relation to the comparison group. In addition, HLA‐B57 was associated with a lower HCV viral load in the control group and HIV controllers, and conversely, HLA‐B35 with higher HCV viral load in HIV controllers. The subrepresentation of HCV genotype 1 and the overrepresentation of HLA‐B57 only partly explained the lower HCV viral load found in HIV controllers. In fact, HIV controller status was independently associated with lower HCV viral load, together with HCV genotype non‐1, the presence of HLA‐B57 and absence of HLA‐B35. Caucasian HIV controllers are able to better control HCV replication, in terms of lower HCV viral load levels. These findings support the idea that some common host mechanisms are involved in the defence against these two persistent infections.     

Sexually transmitted infections and infectiousness beliefs among people living with HIV/AIDS: implications for HIV treatment as prevention

Objectives

Sexually transmitted infections (STIs) significantly impact the health of people living with HIV/AIDS, increasing HIV infectiousness and therefore transmissibility. The current study examined STIs in a community sample of 490 HIV‐positive men and women.

Methods

Assessments were performed using confidential computerized interviews in a community research setting.

Results

Fourteen per cent of the people living with HIV/AIDS in this study had been diagnosed with a new STI in a 6‐month period. Individuals with a new STI had significantly more sexual partners in that time period, including non‐HIV‐positive partners. Participants who had contracted an STI were significantly more likely to have detectable viral loads and were less likely to know their viral load than participants who did not contract an STI. Multivariate analysis showed that believing an undetectable viral load leads to lower infectiousness was associated with contracting a new STI.

Conclusions

Individuals who believed that having an undetectable viral load reduces HIV transmission risks were more likely to be infectious because of STI coinfection. Programmes that aim to use HIV treatment for HIV prevention must address infectiousness beliefs and aggressively control STIs among people living with HIV/AIDS.     

Can community health workers improve adherence to highly active antiretroviral therapy in the USA? A review of the literature

Objectives

Highly active antiretroviral therapy (HAART) has transformed HIV infection into a manageable chronic illness, yet AIDS mortality among ethnic minorities persists in the USA. HAART nonadherence is associated with increased HIV viral load, low CD4 cell count and racial disparities in HIV outcomes. While there is no universal consensus on how to improve medical adherence in HIV‐positive populations, the community health worker (CHW) model is emerging as an effective strategy to overcome barriers to HAART adherence. Although utilized in international settings, there is little evidence regarding the effects of CHWs on HIV outcomes in the USA.

Methods

We performed a comprehensive search from May 2010 to November 2010 to identify studies carried out in the USA that utilized CHWs to improve HAART adherence and measured HIV viral loads and CD4 cell counts to assess intervention effects. Sixteen studies met the inclusion criteria and were reviewed for this article. All studies reported clinical HIV outcomes.

Results

Interventions that lasted at least 24 weeks, provided frequent contact with participants, and focused on medication management were associated with improved HAART adherence, as indicated by reduced HIV viral load and increased CD4 cell count.

Conclusions

Compared with current standards of care, CHW programmes may offer a practical and cost‐effective alternative to improve HAART adherence, which may lead to reduced HIV viral load and increased CD4 cell counts among HIV‐positive populations in the USA.     

Prevalence and clinical characteristics of HIV type 1-infected patients receiving dialysis in Spain: results of a Spanish survey in 2006: GESIDA 48/05 study

End-stage renal diseases (ESRD) are becoming more frequent in HIV-infected patients. In Europe there is little information about HIV-infected patients on dialysis. A cross-sectional multicenter survey in 328 Spanish dialysis units was conducted in 2006. Information from 14,876 patients in dialysis was obtained (81.6% of the Spanish dialysis population). Eighty-one were HIV infected (0.54%; 95% CI, 0.43-0.67), 60 were on hemodialysis, and 21 were on peritoneal dialysis. The mean (range) age was 45 (28-73) years. Seventy-two percent were men and 33% were former drug users. The mean (range) time of HIV infection was 11 (1-27) years and time on dialysis was 4.6 (0.4-25) years. ESRD was due to glomerulonephritis (36%) and diabetes (15%). HIV-associated nephropathy was not reported. Eighty-five percent were on HAART, 76.5% had a CD4 T cell count above 200 cells, and 73% had undetectable viral load. Thirty-nine percent of patients met criteria for inclusion on the renal transplant (RT) waiting list but only 12% were included. Sixty-one percent had HCV coinfection. HCV-coinfected patients had a longer history of HIV, more previous AIDS events, parenteral transmission as the most common risk factor for acquiring HIV infection, and less access to the RT waiting list (p < 0.05). The prevalence of HIV infection in Spanish dialysis units in 2006 was 0.54% HCV coinfection was very frequent (61%) and the percentage of patients included on the Spanish RT waiting list was low (12%).     

Evaluation of the possible influence of hepatitis C virus and liver fibrosis on HIV type 1 immunological and virological outcomes

Objectives The aim of the study was to evaluate the possible effect of hepatitis C virus (HCV) coinfection on the viroimmunological outcomes of HIV‐1 infection. Methods A cross‐sectional study of 805 patients with active HCV infection receiving or not receiving antiretroviral therapy (ART) was carried out. Results A number of parameters were significantly associated with undetectable HIV‐1 viral load in univariate analyses, such as age, toxic habits, CD4 cell count, liver test results, HCV viral load and ART. However, only current ART (P<0.0001), CD4 cell count (P<0.0001), age (P=0.004) and current injecting drug use (P=0.02) were independently associated with undetectable viral load in multivariate analysis. None of the many HCV‐ and liver fibrosis‐related parameters analysed showed a significant association with HIV‐1 viral load or CD4 cell count in multivariate analyses, with the exception of the annual fibrosis progression index which almost reached statistical significance in the subgroup of ART‐untreated patients (P=0.06) and was inversely predictive of CD4 cell count in the whole group (P=0.007). However, its relative weight was modest, as it only explained 0.8% of the total variability in CD4 cell count. Conclusions HCV‐related parameters did not significantly affect virological and immunological outcomes of HIV‐1 infection in ART‐treated and untreated patients. In contrast, liver fibrosis, as measured using the annual fibrosis progression index, was inversely associated with CD4 cell count, although its weight was relatively small. Therefore, HCV‐ and liver fibrosis‐related factors do not seem appreciably to influence these outcomes from a practical viewpoint in ART‐naïve patients, nor impair CD4 and HIV‐1 viral load responses to ART.     

Better preserved immune responses after immunization with rgp 160 in HIV-1 infected patients treated with highly active antiretroviral therapy than in untreated patients with similar CD4 levels during at 2 years' follow-up

Objective

To study the impact of effective highly active antiretroviral therapy (HAART) on the preservation of long‐term CD4 memory cells induced by vaccines in HIV‐1‐infected patients.

Methods

Thirty HIV‐1‐positive patients on HAART with undetectable viral load were randomized into three groups: 10 received HIV‐1 rgp160 vaccine, 10 received tetanus vaccine and 10 patients were not immunized. As controls, 10 HIV‐negative volunteers were immunized with tetanus vaccine. The results were compared with an rgp160 vaccine study performed before the era of HAART on patients with comparable CD4 levels. All patients were monitored for 2 years for T‐cell proliferative responses, T‐cell subset levels, serum IgG and viral load.

Results

After 1 year all patients immunized with rgp160 had strong T‐cell responses to the rgp160 antigen. After 2 years this response was preserved in the HAART‐treated group, but not in the rgp160 immunized non‐HAART group, despite comparable CD4 levels. Recall effects of the CD4‐specific responses towards other antigens were seen in the rgp160‐immunized HAART group.

Conclusion

Immunization with rpg 160 leads to positive effects on HIV‐specific T‐cell proliferative responses in patients both with and without HAART. Immune responses after immunization is better preserved in HAART‐treated patients who have low viral amounts than in individuals with high viral load and no HAART despite comparable CD4 levels during 2 years' follow‐up. Interruption of HAART with return of a high viral load might thus have negative effects on T‐cell functions in the long term, even if CD4 levels are kept at clinically acceptable levels.

     

Plasma Exchange for the Treatment of Human T‐Cell Lymphotropic Virus Type 1 Associated Myelopathy

Abstract: A 55‐year‐old man was admitted to our hospital because of myelopathy. He had a history of chronic renal failure due to polycystic kidney disease at the age of 39, being treated by hemodialysis for 9 years with several blood transfusions for the treatment of renal anemia. After cadaver renal transplantation at the age of 48, he discontinued hemodialysis. At 50 years of age, he had pulmonary tuberculosis and tuberculous arthritis of the left elbow joint. He has experienced difficulty in walking since he was 48 years old, with mild dysuria. Gait disturbance gradually aggravated after that, and urinary retention was observed. When he was 55 years old, being human T‐cell lymphotropic virus type‐1 (HTLV‐1)‐positive in the serum and cerebrospinal fluid, he was diagnosed as having HTLV‐1‐associated myelopathy (HAM). As active steroid therapy was unapplicable because of the history of pulmonary tuberculosis and immunosuppression for transplanted kidney, a series of plasma exchanges (PE) was performed with fresh frozen plasma as a replacement fluid. After PE, dyskinesia of the left leg and dysuria subjectively and objectively improved. These results suggest that PE seems to be one of the therapeutic tools for the treatment of HAM.     

Food insecurity may lead to incomplete HIV viral suppression and less immune reconstitution among HIV/hepatitis C virus‐coinfected people

Objectives

The aim of this study was to determine the impact of food insecurity (FI) on HIV viral load and CD4 count among people coinfected with HIV and hepatitis C virus (HCV).

Methods

This study was conducted using data from the Food Security & HIV‐HCV Sub‐Study of the Canadian Co‐Infection Cohort study. FI was measured using the adult scale of Health Canada's Household Food Security Survey Module and was classified into three categories: food security, moderate food insecurity and severe food insecurity. The association between FI, HIV viral load, and CD4 count was assessed using a stabilized inverse probability weighted marginal structural model.

Results

A total of 725 HIV/HCV‐coinfected people with 1973 person‐visits over 3 years of follow‐up contributed to this study. At baseline, 23% of participants experienced moderate food insecurity and 34% experienced severe food insecurity. The proportion of people with undetectable HIV viral load was 75% and the median CD4 count was 460 [interquartile range (IQR): 300–665] cells/μL. People experiencing severe food insecurity had 1.47 times [95% confidence interval (CI): 1.14, 1.88] the risk of having detectable HIV viral load and a 0.91‐fold (95% CI: 0.84, 0.98) increase in CD4 count compared with people who were food secure.

Conclusions

These findings provide evidence of the negative impact of food insecurity on HIV viral load and CD4 count among HIV/HCV‐coinfected people.

     

Slower fibrosis progression in HIV/HCV-coinfected patients with successful HIV suppression using antiretroviral therapy

BACKGROUND/AIMS: HIV/HCV-coinfected patients reportedly have a faster fibrosis progression rate (FPR) than HCV-monoinfected patients. This study examined whether HIV suppression through highly active antiretroviral therapy (HAART) attenuates this accelerated fibrosis progression. METHODS: In two hepatitis C centers, a retrospective analysis identified 656 consecutive treatment-na?ve HCV-infected patients who had undergone a liver biopsy, had a presumed date of HCV infection, and had been tested for HIV, 274 of them HIV-positive (95.2% on HAART) and 382 HIV-negative. The primary outcome measure was the FPR, defined as Ishak fibrosis score [0-6] over estimated duration of HCV infection. RESULTS: Among HIV/HCV-coinfected patients, 51.2% had undetectable HIV RNA (< 400 copies/mL). There was no difference in FPR between HIV/HCV-coinfected and HCV-monoinfected patients (0.136 vs. 0.128 Ishak fibrosis units/year, P=0.29). However, HIV/HCV-coinfected patients with any detectable HIV viral load >400 copies/mL had a faster FPR (0.151) than HCV-monoinfected patients (0.128, P=0.015) and than HIV/HCV-coinfected patients with undetectable plasma HIV RNA (0.122, P=0.013) who in turn had the same FPR as HCV-monoinfected subjects (0.128, P=0.52). An accelerated FPR in HIV viremic patients was seen with CD4+ cells <500/mm(3) (0.162 vs. 0.123, undetectable HIV RNA, P=0.005) but not with CD4+ cells >500/mm(3) (0.118 vs. 0.121, P=0.89). In multivariable linear regression analysis of HIV/HCV-coinfected patients, log(10) HIV RNA level, necroinflammation, and age at HCV infection were independently correlated to FPR, but not alcohol use or CD4+ cell count (r(2)=0.45 for model). CONCLUSIONS: HIV/HCV-coinfected patients with undetectable HIV RNA through HAART have a slower FPR than those with any HIV RNA level and an FPR similar to HCV-monoinfected individuals.