SVR medicine is a type of antiviral medication that is used to treat viral infections.

SVR medicine is effective against a variety of viral infections.

SVR represents the fundamental goal of antiviral treatment for patients infected with chronic HCV, so as to reduce risk of liver disease progression. Achievement of SVR has implications beyond those of clearing viral infection; it is associated with improved long-term clinical outcomes, economic benefits and improved health-related quality of life.
Antiviral therapy with attainment of sustained virological response (SVR), which is considered to be virological cure, has several hepatic benefits such as normalization of liver enzymes, halting the progression of liver disease, reduction in the risk of hepatocellular carcinoma.
SVR was first achieved in 1986 using interferon; ribavirin (Virazole) was added in later regimens. Complex treatment protocols often caused severe adverse effects and were less effective against certain viral genotypes.4 Currently recommended treatments use direct-acting antivirals. When used for the specified durations, these medications consistently achieve SVR12 rates at or above 90%, and the newest agents are effective against all HCV genotypes 5–10(Table 111).
The therapy of HCV infection is basically aimed to eradicate the virus and prevent the ensuing disease complications. The success of therapy is monitored by SVR rate which is defined as the absence of the HCV RNA in serum post 24 weeks of stoppage of treatment.
The value of SVR indicated not only eradication of virion from circulation but also correlates with symptoms[124. The combination of PegIFN and ribavirin has been the SOC for all patients infected with HCV irrespective of viral genotypes. This regimen produces SVR to 70%-80% in patients with HCV genotype-2 or -3 infection.
However, SVR reached only 45%-70% in patients infected with other genotypes. In recent trials of boceprevir and telaprevir in patients with cirrhosis it was noted that SVR was low in comparison to that in non-cirrhotic patients.
In chronic HCV infection, therapy-induced SVR is a clinically meaningful end point (Table 4). SVR is a durable marker of viral eradication, because evidence for extrahepatic residual viremia is limited, and multiple reports demonstrate that late relapse is rarely observed; SVR is tantamount to cure.
Besides posttherapy improvement in hepatic histologic damage, it is likely that SVR-achieving patients have a diminution in HCV-related insulin resistance and in diabetes development and, relative to therapy nonresponders, have a striking reduction in liver-related complications and mortality.
The goal of chronic hepatitis C treatment is to remove the virus to avoid progression of HCV-related disease. Sustained virologic response (SVR) is the most widely used efficacy endpoint in clinical studies of hepatitis C, and represents the eradication of HCV from the body. The aim of the current review was to examine the long-term clinical, economic and quality of life benefits associated with achieving SVR.
In addition to antiviral agents described above, vitamin B12 was also reported to act as an inhibitor of HCV replication. The use of vitamin B12 with SOC drugs raised the SVR rate to the level higher than the rate noted in patients treated with SOC alone. Recently, it has been observed that vitamin D also acts against HCV in vitro. The SVR rate of patients infected with HCV genotype-1 or 2/3 is improved once vitamin D is added to PegIFN-α and ribavirin therapy[36. A comparison of study using PegIFN-α and RBV with supplement of L-carnitine group vs. the PegIFN-α plus RBV group has shown an increase in SVR rate. This substantiates that L-carnitine may be useful for the treatment of HCV infection.
The effectiveness of antiviral treatment, the extent to which treatment can clear viral infection is assessed according to the proportion of patients achieving sustained virologic response (SVR). SVR is the fundamental goal of treatment and is defined as undetectable (or below the lower limit of quantification) HCV RNA at 12–24 weeks after cessation of treatment [3. SVR rates with a DAA in combination with pegIFN plus ribavirin (PR) currently range from approx. 80–90% for treatment-naïve patients [5, whilst SVR rates of up to 99% have been reported with combinations of two DAAs . Similarly, SVR rates of up to 99% have been reported in treatment-experienced (non-responders and relapsers) patients treated with two-DAA combinations .
For HCV-monoinfected patients with genotype 1 infection (the most common US isolate), the current standard of care, pegylated interferon with ribavirin, yields relatively low SVR rates (42%–46%) [8. Clearly, additional effective therapies are warranted. Insights into HCV virology have identified viral targets for potential novel therapeutics.
This new approach to HCV therapy uses a direct antiviral mechanism and has been deemed directly acting antiviral therapy (DAA). The HCV NS3 protein, in addition to its cofactor NS4A, form a serine protease that cleaves the posttranslational HCV polyprotein into 4 nonstructural proteins. One of these proteins is NS5B, which encodes the HCV RNA polymerase.
Furthest along in DAA development are 2 NS3/4A protease inhibitors that have recently completed phase 3 trials and may be approved this year in combination with pegylated interferon with ribavirin. SVR rates for genotype 1–infected treatment-naive monoinfected patients are as high as 66%–75% with triple combination therapy [124.
The SVR rate for patients infected with HCV genotype 2 and treated with SOC is almost 80%. There is no space for DAAs to show any increase of treatment effect because it is enough high. DAAs may be less effective in this patient group than in patients infected with HCV genotype 1. TVR, the first agent to directly target viral replication, is effective against HCV-2 but not against HCV-3 (see below).
Foster et al. evaluated combined treatment with TVR plus PegIFN-α-2a and RBV in five patients infected with HCV-2 and compared the results with those obtained after treating nine patients with TVR alone or treating nine patients with PR (control group).
Triple combination therapy yielded an SVR rate of 100%, which is remarkable considering the 89% rate observed in patients receiving standard PR . Other NS3/4A protease inhibitors, nucleoside and non-nucleoside reverse replicase inhibitors, and NS5A inhibitors have antiviral activity against HCV-2. One of the most promising drugs is a nucleotide analogue polymerase inhibitor called PSI-7977 . An open-label study (the PROTON study) evaluated the efficacy of PSI-7977 in 15 patients infected with HCV-2, in 10 patients infected with HCV-3, and in a larger group of patients with HCV-1 infection . That study reported an RVR of 96% after the triple combination of 400 mg of PSI-7977 plus PR. Twenty-four HCV-2 and HCV-3 patients who completed the 12 weeks of treatment achieved SVR (96%).
SVR medicine can be taken with or without food.
Certain medicines should not be used at or around the time of eating food or eating certain types of food since interactions may occur. Using alcohol or tobacco with certain medicines may also cause interactions to occur. Discuss with your healthcare professional the use of your medicine with food, alcohol, or tobacco.
Below, the term pegylated interferon refers to either peginterferon alfa-2a 180 µg subcutaneously (SC) once weekly or peginterferon alfa-2b 1.5 µg/kg SC once weekly. Note that peginterferon is contraindicated for use in patients with hepatic decompensation (eg, the presence of ascites). Such patients may be at risk for worsening liver function or sepsis if treated with peginterferon.
Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are taking this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive.
To raise an effective barrier to resistance emergence and to ultimately achieve SVR without interferon, 2 DAAs may be required. Compensatory mutations occur within days of drug exposure because of the drugs’ selective pressure. It is estimated that, for a regimen composed of only DAAs, a barrier of ≥4 mutations is likely to be required to prevent resistance-induced loss of virologic control and, thus, engender SVR .
Peginterferon injection combined with ribavirin can temporarily lower the number of white blood cells in your blood, increasing the chance of getting an infection. It can also lower the number of platelets in the blood, which are necessary for proper blood clotting. If this occurs, there are certain precautions you or your child can take, especially when your blood count is low, to reduce the risk of infection or bleeding:
The effects of therapy on reducing liver disease complications and, therefore, mortality, have been difficult to prove. A multitude of studies have shown that liver-related complications, including decompensation, hepatocellular carcinoma, and liver-related death, are less frequent in sustained virologic responders relative to nonresponders or compared with those untreated (Table 3); however, most data are derived from uncontrolled, largely retrospective analyses with relatively short follow-up periods, compared with the protracted natural history of HCV infection. Because studies were not randomized, prognostic factors, such as alcohol use or even coffee consumption , might have contributed to differences between sustained responders and nonresponders. In some studies, variables that affect clinical event frequency, such as serum bilirubin , were disparate between nonresponders and SVR achievers. Furthermore, selection bias was likely present, because some cirrhotic patients were probably considered to be too ill for treatment and were excluded from these analyses.
The ribavirin dose is based on weight. The initial clinical trials with peginterferon alfa-2a utilized ribavirin at a dose of 1000-1200 mg per day (in two divided doses), whereas the initial clinical trials with peginterferon alfa-2b utilized ribavirin at a dose of 800-1400 mg per day. Trials published in relatively recent years that studied sofosbuvir utilized ribavirin using the following schedule: for individuals weighing less than 75 kg, ribavirin 400 mg in AM and 600 mg in PM; for individuals weighing 75 kg or more, ribavirin 600 mg twice per day. Trials that studied the elbasvir/grazoprevir combination used a different schedule: for individuals weighing less than 66 kg, ribavirin 800 mg per day; for individuals weighing 66 to 80 kg, ribavirin1000 mg per day; for individuals weighing 81 to 105 kg, ribavirin1200 mg per day; for individuals weighing more than 105 kg, ribavirin 1400 mg per day.
Children 3 years of age and older—Dose is based on body weight and must be determined by your doctor. The dose is usually 15 milligrams (mg) per kilogram (kg) of body weight per day, given in 2 divided doses and taken in the morning and evening. Each capsule contains 200 mg of ribavirin.
The major adverse effect of adefovir is nephrotoxicity, including proximal renal tubular dysfunction and Fanconi syndrome. Gastrointestinal symptoms, such as nausea, diarrhea, and abdominal pain, may be observed. Adefovir resistance, characterized by the rtN236T mutation, gradually increases over time to 11%, 18%, and 29% at year 3, 4, and 5, respectively.166-169 To minimize the risk of resistance, adefovir is used in combination with other drugs such as lamivudine.165 However, concomitant use with the related drug tenofovir disoproxil fumarate is not recommended because of the augmented risk of nephrotoxicity.
The Viekira Pak package insert was amended in October 2015. Several cases of hepatic decompensation and death were reported after PrOD therapy was initiated in patients with moderate to severe hepatic impairment (Child-Pugh B and C). The use of PrOD is now contraindicated in these groups.
SVR medicine is safe to take over a long period of time.
In a follow-up period of up to 48 weeks after SVR achievement with pegylated interferon with ribavirin and a protease inhibitor in phase 2 trials, no cases of late relapse had yet occurred [134. Nonetheless, long-term prospective data will be needed to confirm equivalence to SVR with the current standard of care. It is hoped that all the aforementioned benefits of SVR will be better championed by DAAs in the pipeline that will improve SVR rates among patients, particularly those who heretofore had been deemed as difficult to treat.
Most quality of life studies included in the review assessed HRQoL within the first year following treatment; however two studies assessed the impact of SVR at 3 years after completion of antiviral therapy. Both Mauss et al. and John-Baptiste et al. reported that the HRQoL benefits of SVR persist over 3 years, with both studies showing that patients with SVR had significantly better scores in all eight domains of the SF-36 in comparison with those who had failed treatment.
Both Mauss et al. and John-Baptiste et al. also showed that SVR was associated with long-term benefits in terms of work productivity. Mauss et al. reported that a significantly higher proportion of patients who achieved SVR were employed (56%) in comparison with non-SVR patients (41%; p. Similarly, John-Baptiste et al. reported employment figures of 67% for patients with SVR versus 51% for those who failed treatment (p = 0.02). This analysis also showed that long-term work and leisure capacity were significantly compromised in treatment failures in comparison with the SVR group. Treatment failures had a mean (SD) reduction in work capacity of 5.8 (18)%, versus 1.1 (6)% for SVR; the corresponding figures for reduction in leisure capacity were 10.7 (24)% and 3.3 (13%), respectively .
The clinical benefits associated with the achievement of SVR translate into clinically meaningful benefits for patients by improving symptoms, functioning and health related quality of life, compared with those not able to achieve SVR. The findings of quality of life studies consistently showed that patients with SVR had higher utility values and SF-36 and EQ-5D scores in comparison with those who did not respond to treatment. However, in the literature review it was noted that there is a paucity of quality of life studies with long-term follow-up (≥5 years). Although SVR leads to improved quality of life in the short-term, data relating to whether or not this improvement persists in the long term are lacking.
SVR is durable with late relapse rates over 4–5 year periods being in the range of 1–2%. Patients who achieve SVR frequently demonstrate some regression of fibrosis/cirrhosis and have a substantially reduced risk for hepatocellular carcinoma (relative risk [RR] 0.1–0.25), liver-related mortality (RR 0.03–0.2) and overall mortality (RR 0.1–0.3) in comparison with no treatment or treatment failure. In the 5 years post-treatment, medical costs for patients achieving SVR are 13-fold lower than patients not achieving SVR. Patients who achieve SVR also have health state utility values that are 0.05 to 0.31 higher than non-responders to treatment.
To help clear up your infection completely, ribavirin must be given for the full time of treatment, even if you or your child begins to feel better after a few days. Also, it is important to keep the amount of medicine in your body at a steady level. To help keep the amount constant, ribavirin must be given on a regular schedule.
Skipping doses or starting and stopping an antiviral medicine can allow a virus to change/adapt so that the antiviral is no longer effective. This is antiviral resistance. People who take antivirals for extended periods are more prone to antiviral resistance.
It is not clear whether the high cost of direct-acting antivirals is offset by long-term savings related to reduced morbidity and mortality from hepatitis C. Economic estimates vary by health system and by type of study analysis (e.g., whether the study end point is focused on achieving SVR or on post-SVR improvements in HCV-related extrahepatic disease).16–19 A typical treatment course is one to three pills per day for eight to 12 weeks, and is usually well tolerated. Viral counts are obtained at four weeks to assess effectiveness. A final test is performed 12 weeks or more after the last pill is taken. Guidelines recommend that patients with pretreatment evidence of cirrhosis have lifelong surveillance for hepatocellular carcinoma using liver imaging and α-fetoprotein testing at six-month intervals.20 Prior HCV infection and treatment do not confer immunity, so patients at high risk of reinfection (e.g., those with active injection or intranasal drug use, sex partners of infected persons) should be screened periodically.21
Faldaprevir (BI201335) is another NS3/4A protease inhibitor that has completed phase II testing (the SILEN-C1 study) and can be administered using a once-per-day dosing schedule. The treatment regimen included BI201335 in addition to PR for 24 weeks at doses of 120 and 240 mg, followed by another 24 weeks of standard therapy . The overall SVR rate was 83% for the 240 mg dose. Ninety-two percent of the patients that showed an eRVR also achieved an SVR, regardless of the duration of subsequent PR therapy. Adverse events (mostly gastrointestinal) meant that treatment was discontinued in 7.3% of subjects.
Using this medicine while you are pregnant can harm your unborn baby. If you are a woman who can bear children, your doctor may give you a pregnancy test before you start using this medicine to make sure you are not pregnant. This medicine may also cause birth defects if the father is using it when his sexual partner becomes pregnant. Female patients should use an effective form of birth control during treatment with this medicine and for at least 9 months after the last dose. Male patients who have female partners should use effective birth control during treatment with this medicine and for at least 6 months after the last dose. If you think you have become pregnant or your partner has become pregnant while using this medicine, tell your doctor right away.
To date, the vast majority of clinical trials in HCV, including phase III trials of boceprevir and telaprevir, have used SVR at 24 weeks after the planned end of treatment (SVR24) as the primary endpoint. However, research in the field of HCV is currently advancing at a rapid pace and SVR 12 weeks after the end of treatment is now used as the primary endpoint in most clinical studies.
The concordance between SVR12 and SVR24 rates has been investigated, and a high level of concordance was observed, suggesting that SVR12 represents a valid clinical endpoint [13. Specifically, analysis was performed by the FDA in which data from fifteen Phase 2 and 3 trials (n = 12,000 patients) were combined to assess the concordance between SVR24 and SVR12. This analysis showed that concordance was observed between SVR12 and SVR24 for all treatments: 98% of patients with SVR212 had SVR24 .