Acute Hepatitis C in Patients with HIV

• Epidemiology
• Case Definition
• Natural Course
• Treatment Initiation
• Treatment Type
• Treatment Duration
• Conclusion
• Abbreviations
• References

Abstract

Almost 10 years ago clinicians started to note the first cases of an outbreak of acute hepatitis C (AHC) infections among human immunodeficiency virus- (HIV-) positive men who have sex with men (MSM) in Europe, soon followed by similar reports from the United States and Australia. In the absence of randomized controlled treatment trials in AHC, coinfection expert consensus recommendations based upon published data from uncontrolled clinical and cohort studies give guidance on best clinical management. Pegylated interferon in combination with weight-adapted ribavirin is still recommended as the treatment of choice for all HCV genotypes. For patients developing a rapid virologic response, treatment duration of 24 weeks is recommended. If antiviral therapy was initiated within 24 weeks after diagnosis, high sustained virologic response rates of 60 to 80% have been observed. Prevention and screening efforts along with early anti-HCV therapy have to be intensified to allow for control of viral dissemination as the current epidemic of AHC particularly among MSM is still ongoing.

Epidemiology

An increase in acute hepatitis C (AHC) infections among human immunodeficiency virus- (HIV-) positive men who have sex with men (MSM) was first seen in Europe 10 years ago, shortly joined by similar observations in the United States and Australia, as well as other countries such as Canada, Lebanon and Taiwan (see [Fig. 1]).[1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32] [33] [34] Soon it became clear that these cases of AHC were not due to classic hepatitis C virus (HCV) transmission risk factors in populations at risk, but rather seemed to be linked to unsafe sex and recreational drug use (in particular, sexual practices with a high risk for blood–blood contacts including fisting, unprotected anal sex, and nasal snorting of drugs), which were previously considered rare and inefficient transmission routes.[35] Compared with HIV-positive patients without a history of AHC infection, patients with AHC were more likely to engage in sexual practices with a higher risk for mucosal damage, such as receptive fisting, use of dilative sex toys, use of phosphodiesterase 5 inhibitors (e.g., sildenafil), and group sex.[35] Patients also more often reported frequent sexually induced anal bleeding, suggesting that indeed sexual transmission of hepatitis C in this group of patients may occur via blood-to-blood rather than permucosal contact. Behavioral studies also identified a high rate of noninjecting drug use among patients with AHC infection. Sniffing drugs such as cocaine may damage nasal mucosa and transmit HCV by sharing implements for sniffing. Using drugs while having sex may alter level of consciousness and nociception, putting the user at higher risk for mucosal trauma. This overlapping of risk factors may also be an important aspect in transmitting AHC infection via the sexual route. Within the German behavioral study,[35] 30% of patients with sexually transmitted AHC infection reported two or three risk factors, whereas this was only reported from 6% of the controls. Even though the vast majority of sexually transmitted AHC infections has been reported among HIV-positive MSM, acute HCV infections have also been observed in HIV-negative MSM[36] and heterosexual couples.[37]

In contrast to HIV-positive patients who are seen every 3 to 6 months for routine control of HIV infection, HIV-negative patients may consult with their general practitioner on a less-frequent basis, thus acute liver transaminase elevations and diagnosis of asymptomatic acute HCV infection may possibly be missed in the HIV-negative population. Therefore, a certain degree of underreporting must be acknowledged, which may in part explain the lower incidence of acute HCV infections in HIV-negative MSM.

Although sexual transmission of HCV in serodiscordant heterosexual couples has been inefficient with a lifetime risk less than 1%,[38] [39] reported sexual risk factors have been increasing in a recent U.S. report on acute HCV.[40] Although a history of intravenous (IV) drug abuse was still reported most frequently by 48% of study participants, 42% of the participants reported more than one sex partner and 10% revealed their sexual preference as MSM.

The broader availability of lifestyle drugs such as sildenafil and use of noninjecting drugs has influenced sexual culture and has been shown to significantly increase the risk for HIV and other sexually transmitted diseases, not only in MSM but also in other populations.[41] [42] Of interest, in the first case series from the Netherlands[43] a cluster of lymphogranuloma venereum was reported among AHC coinfected patients, and subsequent outbreaks similarly reported a high incidence of concurrent ulcerative bacterial sexually transmitted diseases such as syphilis or gonorrhea. Furthermore, transmission seems to occur via social networks separate from IVDU. Phylogenetic analyses identified MSM-specific clustering of HCV strains with almost three quarters of HCV strains found in Europe circulating in more than one country. Notably, viral sequences from IV drug users or endemic HCV strains were not part of any of these clusters.[44] [45] Additionally, phylogenetic analyses of the Australian Trial in Acute Hepatitis C (ATAHC) in which a significant proportion of MSM self-reported IV drug abuse as the most likely route of hepatitis C transmission revealed MSM-specific clustering regardless of the underlying mode of transmission.[16]

Clearly, with the emergence of this new disease entity in HIV-positive patients new algorithms for best diagnostics, management, and treatment of AHC infections in HIV-positive patients are urgently needed. But data from randomized controlled clinical trials to inform guidelines on best clinical management have not been generated yet. However, over the last years a substantial amount of clinical and cohort studies have provided many insights into the definition of AHC cases, rates of spontaneous viral clearance in the setting of chronic immunosuppression—and last but not least—the type, timing, and duration of antiviral treatment of AHC in HIV coinfection.

Case Definition

AHC infection is defined as the first 6 months of detectable HCV-ribonucleic acid (RNA) in the serum of a patient. As there is a lack of evidence on when acute infection becomes chronic and determining the exact time point of infection is usually difficult, this definition is arbitrary. In addition, timely diagnosis is problematic because the majority of individuals with acute HCV infection are asymptomatic. Only one third to a half of individuals with AHC infection show signs of an acute illness.[5] [11] Anti-HCV seroconversion may be significantly delayed in HIV-positive patients as well, with 5% of cases still anti-HCV negative despite ongoing viral replication for 1 year.[46] However, three monthly alanine aminotransferases (ALT) measurements followed by HCV-RNA testing in cases of suspected AHC seems to be a reasonable approach for AHC screening in HIV-positive individuals and at-risk populations. This recommendation derives from findings from the British St. Mary's Acute Hepatitis C Cohort (SMACC), where 88% of patients experienced elevated ALT within 3 months of infection with peak ALT levels >5 times the upper limit of normal in 55%.[5] [46] [47] If results from past HCV testing are not available, experts recommend to consider newly diagnosed hepatitis C infection acute if ALT levels are more than 10 times the upper limit of normal in the case of no past ALT values available or more than five times the upper limit of normal in the case of documented past normal ALT values. With regards to frequently observed flares of ALT in patients with chronic HCV, we know from cohort data that in less than 2% of cases HIV-infected patients with chronic HCV develop hepatic flares with a rise of ALT >5× ULN (upper limit of normal),[48] which significantly reduces the possibility of classifying chronic HCV infection as acute.

Of note, clinicians worldwide start to notice a second wave of AHC in HIV-infected individuals who had been successfully treated for their first episode of AHC in the past.[49] Recent data from a small Dutch cohort showed reinfection with HCV in 7 out of 26 HIV-positive individuals within 1 year of follow-up.[50] This area clearly needs further study to identify risk factors for reinfection.

Natural Course

Rates of spontaneous HCV clearance have been estimated to be as high as 25% of cases in cohorts focusing on treatment of ACH,[51] while data from cohorts focusing on diagnostics and epidemiology have shown lower rates around 15%.[46] [52] [53] In the Johns Hopkins cohort of predominantly black men with prior or current IVDU, HCV-RNA clearance was observed in 14% of HIV uninfected and 7% of HIV infected.[54] Spontaneous HCV-RNA clearance was higher with 23% in 1940 HCV antibody-positive individuals from the EuroSIDA cohort, but most of the patients very likely acquired their HCV infection prior to becoming HIV seropositive.[15]

Scientific interest is still high in identifying predictors of viral clearance as this would allow clinicians to expose only those of their patients to antiviral therapy who would not clear HCV spontaneously. Unfortunately, most of these studies lack power due to small numbers of patients to accurately distinguish between predictive factors. For example, both of the above-mentioned cohorts identified different factors associated with spontaneous HCV clearance including non-black ethnicity, younger age (<45 years), HBsAg positivity, female sex, mode of transmission (sexual vs IVDU), and region (other European regions vs southern Europe/Argentina). Additionally, high ALT and CD4 cell count have been described as predictors for spontaneous clearance in two studies.[55] [56] The strongest evidence comes from genome-wide association studies in HCV monoinfection, which identified single-nucleotide polymorphisms (SNP) near the IL28B gene encoding for interferon lambda that comprise a crucial part of the host's innate immune defense against HCV.[57] [58] [59] Individuals with the CC genotype were more than three times likely to clear HCV-RNA compared with individuals with C/T and T/T genotypes.[51] [57] Similar observations have been made in HIV/HCV coinfected individuals.[17] [31] Interestingly, these SNPs could explain differences in spontaneous clearance rates between races as the frequency of the protective allele varies across ethnic groups with a lower frequency in those of African origin compared with European patients.[57]

To date, inconclusive data exist on liver fibrosis progression after AHC in HIV coinfection. Cohort data from the United States showed moderately advanced fibrosis in liver biopsy of 82% of patients (n = 11) with higher age, longer duration of HIV infection, and longer exposure to antiretroviral therapy (ART).[60] Additionally, recent data from the European AHC Cohort should ease patients and clinicians about the risk of liver cirrhosis after AHC as the investigators found no evidence for a fastened fibrosis progression rate assessed mainly by transelastography in 45 patients over a median follow-up of 6 months after diagnosis of AHC.[61]

To further investigate into the epidemiology, natural history, and treatment outcomes of AHC infection in a more meaningful setting, the European AIDS Treatment Network (NEAT) group has recently opened a multicenter, prospective cohort study for recruitment, in which 600 HIV-positive and -negative patients with documented AHC infection will be followed prospectively over an initial period of 3 years after diagnosis of AHC infection (PROBE-C study, ClinicalTrials.gov Identifier: NCT01289652).

Treatment Initiation

Also of high clinical significance is the determination of the point in time until which spontaneous clearance can be expected and subsequent treatment can be postponed without impeding its efficacy. Several cohort data have provided useful answers to the question if it is possible to predict progression to chronicity of AHC infection by looking at the course of HCV-RNA after diagnosis. In a European cohort of 92 HIV-positive patients with AHC who did not receive HCV-specific antiviral therapy, the sensitivity and specificity of HCV-RNA determination 4 and 12 weeks after diagnosis to predict the outcome of AHC was similarly strong.[62] [63] Nine of 10 patients showing spontaneous regression of HCV-RNA of at least 2 log 4 weeks after diagnosis subsequently cleared HCV, whereas 92% of patients who were HCV-RNA-positive 12 weeks after diagnosis developed chronic HCV. Data from another, though small cohort in HIV-negative patients support the definition of 12 weeks HCV-RNA negativity as a predictor of chronicity.[64] In this study, only 2 of 24 cases with spontaneous clearance had HCV-RNA detectable 12 weeks after diagnosis and none after 16 weeks. Further support comes again from the SMACC cohort in which a rapid decline in HCV-RNA (>2 log within 100 days of infection) in 112 HIV-infected patients was also identified as a predictor for spontaneous clearance along with high CD4 T-cell count, elevated bilirubin, and ALT levels.[56]

Comfortingly, a delay of 12 weeks in starting antiviral therapy has been shown to not impair the virologic outcome, e.g., in the HEPNET III cohort (cohort on patients with acute HCV and no HIV)[65] and the ATAHC cohort, where treatment response rates appeared similar in acute or early chronic HCV infection in both HIV-negative and positive patients.[66] In the majority of studies of AHC treatment in HIV-infected patients, treatment was initiated between 12 and 24 weeks after diagnosis.

The procedures for assessment of liver disease stage and control examinations before and during HCV therapy are similar to those in chronic HCV.

In the light of the given data, experts such as the European AIDS Treatment Network (NEAT) acute HCV consensus panel recommend that treatment should be offered to all patients who do not spontaneously show a drop in HCV-RNA of more than 2 log at week 4 or who are still HCV-RNA positive at week 12 after diagnosis (see [Fig. 2]).[68]

Treatment Type

Over the years, reports of cohorts studying treatment of AHC in HIV-infected persons have accumulated (see [Table 1]). Patients were treated with pegylated interferons (pegIFNs) at standard doses (α-2b, 1.5 µg/kg/wk and α-2a, 180 µg/wk); ribavirin (RBV) was used in 85% of patients: weight-adjusted dosing in 84% and fixed dose in 16%. Sustained virologic response (SVR) rates of 60 to 80% after early antiviral therapy with pegIFN and RBV have been shown within these clinical studies and cohorts, regardless of HCV genotype.[1] [32] [33] [55] [69] [70] [71] [72] [73] [74] These rates are clearly higher compared with SVR rates observed in the setting of chronic HCV infection, where rates of around 30% are reached for genotype 1 infection[75] [76] being the predominant HCV genotype in acute HCV infection.

The added value of RBV is still very much in the focus of scientific interest. RBV nonetheless seems to be necessary to reach high response rates in the light of case reports of inefficient pegIFN monotherapy from Germany[69] and a first pilot trial of pegIFN monotherapy from the Netherlands.[77] In addition, RBV's important contribution to improving viral kinetic response has been demonstrated in the above-mentioned ATAHC study, where greater reductions in HCV-RNA were seen between weeks 8 to 12 of treatment in HIV/HCV coinfected patients receiving combination therapy compared with pegIFN alone in monoinfected patients.[78] On the contrary, within the German study on acute HCV in HIV-positive individuals pegIFN monotherapy appeared more effective than pegIFN/RBV combination therapy,[69] [77] although the analysis was performed post hoc and this was not statistically significant.

A different approach was studied in a study from the United States where RBV was stopped early on if HCV-RNA was negative 8 and 12 weeks after the start of antiviral therapy.[79] End-of-treatment data have recently been presented showing high overall SVR rates (62%). Most importantly, all patients who stopped RBV at week 12 achieved SVR justifying further exploration of this kinetically guided, 24-week treatment approach in a larger patient population.[80]

With regard to IL28B's influence on treatment outcome published data from a German cohort showed that in contrast to HIV-infected patients with chronic HCV, the IL28B genotype was not significantly associated with treatment response rates in patients with AHC,[18] [81] which is in line with known data on the effect of IL28B in the treatment of AHC in HIV-negative individuals.[51]

Furthermore, recently presented data from a large European cohort for the first time revealed the beneficial influence of GT ⅔ infection on treatment outcome in the setting of AHC suggesting different cure rates depending on HCV genotype similar to the genotype effects seen in chronic HCV therapy.[27] In this cohort, patients with GT ⅔ infection were almost three times more likely to reach SVR than patients with GT ¼ infection. An interesting finding which clearly needs further confirmation in future studies.

To date, no data exist on the efficacy of specifically targeted antiviral therapy for HCV with the novel HCV protease inhibitors (PIs) in the setting of acute HCV infection as these are just being evaluated in chronic HCV/HIV coinfection and only for genotype 1. On the one hand, results are eagerly awaited as these novel agents have demonstrated promising therapeutic efficacy in large phase II trials. On the other hand, their implementation into clinical practice in the setting of HIV coinfection will be determined by the already known potential for development of HCV protease inhibitor drug resistance mutations (hence no monotherapy feasible), their additive toxicity effects, and their high potential for interactions with antiretrovirals.

Treatment Duration

Analogous to using viral kinetics in predicting spontaneous viral clearance, evidence for the use of viral kinetics in determining the chance of SVR and potentially the optimal length of therapy comes from the European Collaborative Cohort Study.[82] In this observational cohort, patients who were able to achieve a viral load of less than 600 IU/mL at week 4 had a very high chance of reaching SVRs. In contrast, patients who did not reach a viral load of less than 600 IU/mL at week 12 were most likely to fail therapy. An additional subanalysis showed that German patients who were treated for at least 20 weeks or longer following a first HCV-RNA of less than 600 IU/mL had a 96% chance of cure (SVR), whereas only 20% of patients reached SVR if they were treated less than 20 weeks after a first HCV-RNA of less than 600 IU/mL.[82] Although 48 weeks of therapy for acute HCV in HIV-infected patients appeared more efficacious than 24 weeks in another single study,[83] other reports in AHC coinfection showed SVR rates of greater than 70% with no statistically significant difference by length of therapy.[66] [69] [84] Most recent data from the United Kingdom support the rapid virologic response- (RVR-) driven treatment duration as recommended by the NEAT consensus panel.[68] [85]

Of note, modern commercial assays have reached lower limits of detection of HCV-RNA of 10 or 15 IU/mL. Although the value of more sensitive assays for defining virologic response have not been explored thus far in the setting of acute HCV infection, residual viremia below 600 IU/mL at week 4 of treatment has been associated with decreased odds for achieving SVR in the setting of chronic HCV infection.[86]

In summary, experts recommend the use of pegIFN and weight-based RBV for all HIV-positive patients with AHC infection. Stopping RBV after week 12 in patients who have achieved a negative HCV-RNA at week 8 or 12 may be an option for patients experiencing RBV-associated toxicity. Viral decay may be slowed in HIV-positive compared with HIV-negative patients and groups of patients may benefit from prolonged duration of treatment. The NEAT acute HCV consensus panel therefore recommends considering 24 weeks of therapy sufficient if the patients reach RVR; in patients who do not reach RVR, 48 weeks of therapy may be considered.[68]

Conclusion

Transmission of hepatitis C among HIV-positive individuals, especially among MSM, has been increasing and is still ongoing. The rate of spontaneous viral clearance in HIV-positive patients is estimated to be around 15 to 25% of patients. Early antiviral therapy is recommended in patients who do not reach a significant decay of HCV-RNA 4 weeks after diagnosis or who still have detectable HCV-RNA 12 weeks after diagnosis. The current standard regimen to treat acute HCV infection in HIV-positive individuals is pegIFN in combination with weight-based RBV. Duration of treatment should be adjusted on the basis of the initial virologic response to antiviral therapy. Randomized controlled trials are urgently needed to help develop guidelines on best clinical management of AHC coinfection including topics such as usage of newly developed protease inhibitors, added value of RBV as well as influence of HCV genotype and IL28B genotype polymorphism on treatment duration.

Abbreviations

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Address for correspondence and reprint requests

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