Ribavirin (Virazole) Inhalation

Number: 0155


  1. Aetna considers ribavirin (Virazole) medically necessary for the treatment of respiratory syncytial virus (RSV) infection in immunosuppressed and high risk children and adults, and for the treatment of viral hemorrhagic fever (Crimean-Congo, Ebola, Lassa, and Marburg), Rift valley fever and Hantaan, a hanta virus.

  2. Aetna considers ribavirin experimental and investigational for all other indications (e.g., acute myeloid leukemia, foot-and-mouth disease, glioblastomas, hepatitis E infection, multiple sclerosis, oral cancer, parainfluenza viral infections in immunocompromised individuals, and thyroid cancer; not an all-inclusive list) because its effectiveness for indications other than the ones listed above has not been established.

See also CPB 0318 - Synagis (Palivizumab).

Dosing Recommendations

The recommended treatment regimen is 20 mg/mL Virazole as the starting solution in the drug reservoir of the SPAG-2 unit, with continuous aerosol administration for 12-18 hours per day for 3 to 7 days. Using the recommended drug concentration of 20 mg/mL the average aerosol concentration for a 12 hour delivery period would be 190 mcg/L of air.

Source: Virazole Prescribing Information.


Ribavirin is indicated for use in the treatment and prevention of certain viral infections in selected patients.  Ribavirin is marketed as a inhalation solution (Virazole), oral capsule (Rebetol) and tablet (Copegus, Moderiba, Ribasphere/RibaPak), but can also be prepared for intravenous administration. The focus of this CPB is on ribavirin powder for inhalation (Virazole).

Mallet et al (2010) reported 2 patients in whom ribavirin therapy seemed to alter the natural history of chronic hepatitis E virus (HEV) infection.  A kidney and pancreas transplant recipient and a patient with idiopathic CD4(+) T lymphocytopenia, both with biopsy-proven chronic HEV infection were included in this study.  Patients received oral ribavirin, 12 mg/kg of body weight daily for 12 weeks.  Liver function tests, detection of HEV RNA (viremia and stool shedding) by reverse transcriptase polymerase chain reaction, and anti-HEV IgM and IgG antibodies wer performed.  Both patients had normalized liver function test results after 2 weeks of treatment and cleared HEV after 4 weeks of treatment.  Hepatitis E virus RNA remained undetectable in the serum and stools throughout follow-up (3 months and 2 months for the 1st and 2nd patient, respectively).  Side effects were considered mild.  The authors concluded that ribavirin is a potentially effective treatment of HEV infection and should be evaluated in patients with chronic HEV infection.  The main drawback of this study was that given the relatively short follow-up, the achievement of HEV eradication could not be claimed.

In a pilot study, Kamar and colleagues (2010) evaluated the ant-iviral effect of ribavirin monotherapy in patients with chronic HEV infection following kidney transplantation.  A total of 6 patients who received kidney transplants and were positive for HEV RNA (infected with HEV for 36.5 months; [range of 11 to 46 months]) were given ribavirin monotherapy for 3 months.  Ribavirin was given at 600 to 800 mg/day in 2 separate doses, based on the patient's ability to clear creatinine.  Median serum concentration of HEV RNA at baseline was 5.77 log copies/mL (range of 4.35 to 7.35 log copies/ml).  Three months after ribavirin therapy commenced, HEV RNA was undetectable in serum samples from all patients.  A sustained virologic response was observed in 4 patients; the other 2 patients relapsed at 1 and 2 months after ribavirin therapy ended.  At the end of the study, all patients had normal levels of alanine and aspartate aminotransferase.  Anemia was the main side effect caused by ribavirin therapy.  The authors concluded that ribavirin monotherapy inhibits the replication of HEV in vivo and might induce a sustained virological response in patients with chronic HEV infections.  They stated that further studies are needed to determine the optimal duration of ribavirin therapy.

Kamar et al (2014) noted that there is no established therapy for HEV infection.  In a retrospective, multi-center case-series study, these researchers evaluated the effects of ribavirin as monotherapy for solid-organ transplant (SOT) recipients with prolonged HEV viremia.  They examined the records of 59 patients who had received a solid-organ transplant (37 kidney-transplant recipients, 10 liver-transplant recipients, 5 heart-transplant recipients, 5 kidney and pancreas-transplant recipients, and 2 lung-transplant recipients).  Ribavirin therapy was initiated a median of 9 months (range of 1 to 82) after the diagnosis of HEV infection at a median dose of 600 mg per day (range of 29 to 1,200), which was equivalent to 8.1 mg/kg body weight/day (range of 0.6 to 16.3).  Patients received ribavirin for a median of 3 months (range of 1 to 18); 66 % of the patients received ribavirin for 3 months or less.  All the patients had HEV viremia when ribavirin was initiated (all 54 in whom genotyping was performed had HEV genotype 3).  At the end of therapy, HEV clearance was observed in 95 % of the patients.  A recurrence of HEV replication occurred in 10 patients after ribavirin was stopped.  A sustained virologic response, defined as an undetectable serum HEV RNA level at least 6 months after cessation of ribavirin therapy, occurred in 46 of the 59 patients (78 %).  A sustained virologic response was also observed in 4 patients who had a recurrence and were re-treated for a longer period.  A higher lymphocyte count when ribavirin therapy was initiated was associated with a greater likelihood of a sustained virologic response.  Anemia was the main identified side effect and required a reduction in ribavirin dose in 29 % of the patients, the use of erythropoietin in 54 %, and blood transfusions in 12 %.  The authors concluded that the findings of this retrospective, multi-center study showed that ribavirin as monotherapy may be effective in the treatment of chronic HEV infection; a 3-month course seemed to be an appropriate duration of therapy for most patients.

Unzueta and Rakela (2014) stated that HEV infection (genotype 3) has been described in developed countries as a cause of chronic hepatitis in recipients of SOT.  Immunosuppression seems to play a major role in the pathogenesis of chronic infections.  The current gold standard for the diagnosis of HEV infection is the detection of HEV RNA in serum, stools, or both.  In liver transplant recipients, HEV infection is considered an uncommon disease; however, a high index of suspicion is needed for patients with graft hepatitis of an unclear etiology.  Liver transplant recipients seem more likely to develop chronic HEV after an acute infection, and there is accelerated progression to advanced fibrosis and cirrhosis.  A decrease in immunosuppression is considered the first line of treatment, and pegylated interferon can be considered the second line of treatment for liver transplant recipients.  At the present time, there are not enough data to recommend treatment with ribavirin for adult liver transplant recipients, although this has been tried in other SOT populations.

An UpToDate review on "Hepatitis E virus infection" (Umashanker and Chopra, 2014) states that "Case reports and series have suggested a benefit from ribavirin monotherapy in solid-organ transplant recipients with chronic HEV, but prospective studies are needed to confirm these findings and to determine the dose, duration, and timing of ribavirin therapy".

Zhang et al (2015) noted that an estimated 170 million people worldwide are infected with hepatitis C virus (HCV); and HCV genotype 4 (HCV-4) – the most prevalent hepatitis C strain in the Middle East and Africa – is difficult to treat, with an estimated sustained virological response (SVR) of 53 % when using pegylated interferon and ribavirin (P/R) in treatment-naïve patients with HCV-4 infection.  In regions where access to direct-acting anti-virals is limited, re-treatment of patients who failed therapy with another course of P/R may be an option if the success rate is acceptable.  These investigators determined the SVR from re-treatment with P/R in treatment-experienced patients with HCV-4 infection.  They performed a meta-analysis using Medline and Embase searches, and by reviewing article bibliographies and abstracts from recent Liver Society Meetings.  Original studies featuring at least 10 adult, treatment-experienced patients with HCV-4 infection failing prior interferon-based therapy and receiving subsequent re-treatment with P/R were included.  A total of 3 studies were included.  Overall pooled SVR was 32.7 %, or 41/126 patients.  No significant heterogeneity existed among the studies; 1 study reported higher SVR of 50 % in previous relapsers, compared with 23 % in previous non-responders.  The authors concluded that as expected, treatment-experienced patients achieved lower rate of SVR compared with previously reported SVR for treatment-naïve patients with HCV-4 infection.  They stated that the abysmal rate of success from re-treatment with P/R supports the use of direct-acting anti-virals whenever re-treatment is considered, even in resource-limited regions.

Foot-and-Mouth Disease

Choi and colleagues (2018) noted that foot-and-mouth disease (FMD) is a highly contagious viral vesicular disease of cloven hoofed animals caused by the foot-and-mouth disease virus (FMDV), which is one of the highly variable RNA viruses.  In many countries, vaccines are used for the prevention of FMD.  However, because there is no protection against FMD immediately after vaccination, research and development on anti-viral agents is being conducted to induce protection until immunological competence is produced.  Until now, no cases of the use of an instantly effective anti-viral agent in the field for treatment or prevention have been reported.  This study tested whether well-known chemicals used as RNA virus treatment agents had inhibitory effects on FMD viruses (FMDVs) and demonstrated that ribavirin (RBV) showed anti-viral effects against FMDV in-vitro/in-vivo.  In addition, it was found that combining the administration of the anti-viral agents orally and complementary therapy with vaccines synergistically enhanced anti-viral activity and preserved the survival rate and body weight in the experimental animals.  Anti-viral agents mixed with an adjuvant were inoculated intramuscularly along with the vaccines, thereby inhibiting virus replication after injection and verifying that it was possible to induce early protection against viral infection prior to immunity achieved through the vaccine.  Finally, the pigs treated with anti-viral agents and vaccines showed no clinical signs and had low virus excretion.  The authors concluded that based on these results, it is expected that this approach could be a therapeutic and preventive treatment for early protection against FMD.


Ochiai and colleagues (2018) stated that ribavirin has been used as an anti-viral agent against RNA and DNA viruses and has become the standard agent used for chronic hepatitis C in combination with interferon (IFN)-α2a.  Furthermore, the potential anti-tumor efficacy of ribavirin has attracted increasing interest.  Recently, these researchers demonstrated a dose-dependent anti-tumor effect of ribavirin for 7 types of malignant glioma cell lines.  However, the mechanism underlying the anti-tumor effect of ribavirin has not yet been fully elucidated.  These investigators provided further relevant data using 2 types of malignant glioma cell lines (U-87MG and U-138MG) with different expression of MGMT.  Dotted accumulations of γH2AX were found in the nuclei and increased levels of ATM and phosphorylated ATM protein expression were also observed following ribavirin treatment (10 µM of ribavirin, clinical relevant concentration) in both the malignant glioma cells, indicating double-strand breaks as one possible mechanism underlying the anti-tumor effect of ribavirin.  In addition, based on evaluations using FACS, ribavirin treatment tended to increase the G0/G1 phase, with a time-lapse, indicating the induction of G0/G1-phase arrest.  Furthermore, an increased phosphorylated p53 and p21 protein expression was confirmed in both glioma cells.  Additionally, analysis by FACS indicated that apoptosis was induced following ribavirin treatment and caspase cascade, down-stream of the p53 pathway, which indicated the activation of both exogenous and endogenous apoptosis in both malignant glioma cell lines.  The authors concluded that these findings may provide an experimental basis for the clinical treatment of glioblastomas with ribavirin.

Lassa Fever

Eberhardt and colleagues (2019) noted that Lassa fever (LF) causes annual outbreaks in endemic regions with high mortality of symptomatic patients.  Ribavirin is recommended as standard treatment for LF in national and international guidelines; however, the evidence for this recommendation has been questioned recently.  These researchers conducted a systematic review and included 6 studies providing efficacy data of ribavirin treatment for LF.  Besides retrospective case-series studies, the evidence mostly relied on a single, prospective clinical trial with critical risk of bias.  In that trial, LF associated mortality was reduced for patients with elevated aspartate aminotransferase (AST) when treated with ribavirin (odds ratio [OR] 0.41, 95 % confidence interval [CI]: 0.23 to 0.73), while mortality was higher for patients without elevated AST (OR 2.37, 95 % CI: 1.07 to 5.25).  The authors concluded that based on the available data, current treatment guidelines may therefore put patients with mild LF at increased risk of death.  The role of ribavirin in the treatment of LF requires urgent re-assessment.

Parainfluenza Viral Infections in Immunocompromised Patients

Falsey and co-workers (2012) stated that parainfluenza viruses (PIV) are common respiratory viruses that belong to the Paramyxoviridae family; and PIV infection can lead to a wide variety of clinical syndromes ranging from mild upper respiratory illness to severe pneumonia.  Severe disease can be seen in elderly or chronically ill persons and may be fatal in persons with compromised immune systems, particularly children with severe combined immunodeficiency disease syndrome (SCIDS) and hematopathic stem cell transplant (HSCT) recipients.  Currently, there are no licensed anti-viral agents for the treatment of PIV infection.  Aerosolized or systemic RBV in combination with intravenous gamma globulin (IVIG) has been reported in small, uncontrolled series and case reports of immunocompromised patients.  Most of the information regarding the clinical utility of RBV came from case reports or small, uncontrolled series.  In children with SCIDS and PIV infection, aerosolized RBV has been administered over long periods of time (3 to 10 months) without apparent toxicity.  The authors noted that although RBV has been well-tolerated, the efficacy for the treatment of PIV infection is difficult to determine, as most case series involve small numbers, different routes of administration, combination treatment with IVIG, and different patient populations.  The majority of data were in HSCT patients and consensus indicated that RBV is not effective for PIV pneumonia when given late in the course of illness, especially if respiratory failure has ensued.  Some reports suggested a modest benefit if the drug is given at the early stage of upper respiratory tract  infection (URTI), but this is controversial because of the lack of controlled trials.  Most of the studies of HSCT patients reported RBV treatment of both URTI and lower respiratory tract infection (LRTI) of PIV and demonstrated no clear benefit of RBV treatment.

von Lilienfeld-Toal and colleagues (2016) stated community acquired viruses (CRVs) may cause severe disease in cancer patients.  Thus, efforts should be made to diagnose CRV rapidly and manage CRV infections accordingly.  A panel of 18 clinicians from the Infectious Diseases Working Party of the German Society for Hematology and Medical Oncology convened to evaluate the available literature and provided recommendations on the management of CRV infections including influenza, respiratory syncytial virus, parainfluenza virus, human metapneumovirus and adenovirus.  CRV infections in cancer patients may lead to pneumonia in approximately 30 % of the cases, with an associated mortality of around 25 %.  For diagnosis of a CRV infection, combined nasal/throat swabs or washes/aspirates gave the best results and nucleic acid amplification based-techniques (NAT) should be used to detect the pathogen.  Hand hygiene, contact isolation and face masks have been shown to be of benefit as general infection management.  Causal treatment could be given for influenza, using a neuraminidase inhibitor, and respiratory syncytial virus (RSV), using RBV in addition to IVIGs.  The authors stated that RBV has also been used to treat parainfluenza virus and human metapneumovirus, but data were inconclusive in this setting.

Beaird and associates (2016) stated the optimal treatment for RSV infection in adult immunocompromised patients is unknown.  These investigators evaluated the management of RSV and other non-influenza respiratory viruses in Midwestern transplant centers.  A survey assessing strategies for RSV and other non-influenza respiratory viral infections was sent to 13 centers.  Multiplex polymerase chain reaction (PCR) assay was used for diagnosis in 11/12 centers; 8 of 12 centers used inhaled RBV in some patient populations.  Barriers included cost, safety, lack of evidence, and inconvenience; 6 of 12 used IVIG, mostly in combination with RBV.  Inhaled RBV was used more than oral, and in the post-stem cell transplant population, patients with LRTI, graft-versus-host disease (GVHD), and more recent transplantation were treated at higher rates; 10 centers had experience with lung transplant patients; all used either oral or inhaled RBV for LRTI, 6/10 treated URTI.  No center treated non-lung solid organ transplant (SOT) recipients with URTI; 7/11 would use oral or inhaled RBV in the same group with LRTI.  Patients with hematologic malignancy without HSCT were treated with RBV at a similar frequency to non-lung SOT recipients; 3 of 12 centers, in severe cases, treated parainfluenza and metapneumovirus, and 1/12 treated coronavirus.  The authors concluded that treatment of RSV in immunocompromised patients varied greatly.  While most centers treat LRTI, treatment of URTI was variable.  No consensus was found regarding the use of oral versus inhaled RBV, or the use of IVIG.  They stated that the presence of such heterogeneity demonstrated the need for further studies defining optimal treatment of RSV in immunocompromised hosts.

Russell and Ison (2017) noted that PIV is a negative-sense single-stranded RNA virus in the Paramyxoviridae family.  There are 4 serotypes that follow seasonal patterns with varying rates of infection for each serotype.  PIV is an established cause of disease and death in the pediatric and immunocompromised populations, and its impact on the hospitalized adult is becoming more apparent with the increased use of multiplex molecular assays in the clinical setting.  The clinical presentation of PIV in hospitalized adults varied widely and included URTI, severe LURT, and exacerbations of underlying disease; 0.2 % to 11.5 % of hospitalized patients with pneumonia have been found to have PIV infection.  Currently no licensed treatment is available for PIV infection.  Ribavirin has been used, but case studies showed no impact on mortality rates.

Seo and colleagues (2019) stated that PIV infection can progress from URTI to LRT disease (LRTD) in immunocompromised hosts.  Risk factors for progression to LRTD and presentation with LRTD without prior URTI are poorly defined.  Recipients of HSCT with PIV infection were retrospectively analyzed using standardized definitions of LRTD; PIV was detected in 540 HCT recipients; 343 had URTI alone and 197 (36 %) had LRTD (possible, 76; probable, 19; proven, 102).  Among 476 patients with positive nasopharyngeal samples, the cumulative incidence of progression to probable/proven LRTD by day 40 was 12 %, with a median time to progression of 7 days (range of 2 to 40).  In multi-variable analysis monocytopenia (hazard ratio [HR], 2.22; p = 0.011), steroid use of greater than or equal to 1 mg/kg prior to diagnosis (HR, 1.89; p = 0.018), co-pathogen detection in blood (HR, 3.21; p = 0.027), and PIV type 3 (HR, 3.57; p = 0.032) were associated with increased progression risk.  In the absence of all 4 risk factors no patients progressed to LRTD, whereas progression risk increased to greater than 30 % if 3 or more risk factors were present.  Viral load or RBV use appeared to have no effect on progression.  Among 121 patients with probable/proven LRTD, 64 (53 %) presented LRTD without prior URTI, and decreased lung function before infection and lower respiratory co-pathogens were risk factors for this presentation.  Mortality was unaffected by the absence of prior URTI.  The authors concluded that the risk of progression to probable/proven LRTD exceeded 30 % with greater than or equal to 3 risk factors.  To detect all cases of LRTD, virologic testing of lower respiratory samples is needed regardless of URTI symptoms.

Smielewska and associates (2018) evaluated RBV, favipiravir (FVP) and zanamivir (ZNV) as inhibitors of minimally passaged United Kingdom clinical strains of human parainfluenza 3 (HPIV3) as well as a laboratory adapted strain MK9 in-vitro.  The inhibitory action of RBV, FVP and ZNV was evaluated against 9 minimally passaged clinical strains and a laboratory adapted strain MK9 using plaque reduction and growth curve inhibition in a cell culture model.  Clinical isolates were found to be at least as susceptible as the laboratory adapted strains to RBV and FVP and significantly more susceptible to ZNV.  However the inhibitory concentrations achieved by ZNV against clinical strains remain prohibitively high in-vivo; RBV, FVP and ZNV were found to be effective inhibitors of HPIV3 in-vitro.  The lack of efficacy of RBV in-vivo may be due to inability to reach required therapeutic levels; FVP, on the other hand, is a good potential therapeutic agent against HPIV3.  The authors concluded that further studies using wild type clinical strains, as well as better formulation and delivery mechanisms may improve the utility of these 3 inhibitors.

Furthermore, an UpToDate review on "Parainfluenza viruses in adults" (Ison, 2018) states that "There are no antiviral agents with proven efficacy for PIV infections.  We suggest not using ribavirin or intravenous immunoglobulin for the treatment of parainfluenza virus pneumonia given the lack of proven benefit".

Oral Cancer

Dai and co-workers (2017) noted that up-regulation of eukaryotic translation initiation factor 4E (eIF4E) is associated with poor clinical outcome in many human cancers and represents a potential therapeutic target.  However, the function of eIF4E remains unknown in oral tongue squamous cell carcinoma (OTSCC).  In this study, these researchers showed that ribavirin augmented sensitivity of OTSCC cells to paclitaxel via inhibiting mTOR/eIF4E signaling pathway.  Ribavirin dose-dependently inhibited proliferation and induced apoptosis in SCC-9 and CAL27 cells.  Combination of ribavirin and paclitaxel were more effective in inhibiting proliferation and inducing apoptosis in OTSCC cells.  More importantly, the in-vivo efficacy of ribavirin and its synergism with paclitaxel was confirmed by 2 independent OTSCC xenograft mouse models.  Mechanistically, ribavirin significantly decreased mTOR/eIF4E signaling pathway in OTSCC cells via suppressing phosphorylation of Akt, mTOR, 4EBP1 and eIF4E.  Over-expression of the phosphor-mimetic form of eIF4E (eIF4E S209D) but not the non-phosphorylatable form (eIF4E S209A) reversed the effects of ribavirin, confirming that eIF4E inhibition is the mechanism of action of ribavirin in OTSCC cells.  In addition, eIF4E depletion significantly enhanced the anti-proliferative and pro-apoptotic effects of paclitaxel, demonstrating the critical role of eIF4E in OTSCC cell response to paclitaxel.  The authors concluded that this study was the first to demonstrate the efficacy of ribavirin as a single agent and synergism as combination with paclitaxel in OTSCC in-vitro and in-vivo.  They stated that their findings also demonstrated the therapeutic value of inhibiting eIF4E in OTSCC treatment.

Thyroid Cancer

Shen and associates (2017) noted that although eIF4E is important in cancer development and progression, its role in thyroid cancer is not well understood.  Ribavirin has been identified as an eIF4E inhibitor.  These researchers examined the effects of ribavirin on thyroid cancer and its molecular mechanisms of action.  The effects of ribavirin on thyroid cancer was investigated using in-vitro cellular assays and in-vivo xenograft mouse model.  The mechanism of its action on eIF4E-β-catenin axis was examined using genetic and biochemical approaches.  These investigators showed that ribavirin inhibited proliferation and induced apoptosis in the thyroid cancer cell lines 8505C and FTC-133.  Ribavirin inhibited thyroid cancer growth in a xenograft mouse model.  Ribavirin also sensitized thyroid cancer's response to paclitaxel.  Mechanistically, ribavirin suppressed eIF4E phosphorylation and over-expression of its wildtype and phosphor-mimetic form (S209D); but not of the non-phosphorylatable form (S209A), which rescued the inhibitory effects of ribavirin in thyroid cancer cells.  These researchers further demonstrated that ribavirin suppressed phosphorylation and activities of β-catenin and its subsequent gene transcriptional expression. β-catenin over-expression rescued the effects of ribavirin in thyroid cancer cells.  More importantly, they showed that eIF4E regulated β-catenin and that the regulation depended on phosphorylation at S209.  The in-vivo inhibitory effects of ribavirin on phosphorylation of eIF4E and β-catenin were also observed in thyroid tumor.  The authors concluded that these findings demonstrated that ribavirin acted on thyroid cancer cells by inhibiting eIF4E/β-catenin signaling; suggesting that ribavirin has the potential to be re-purposed for thyroid cancer treatment and also highlighted the therapeutic value of inhibiting eIF4E-β-catenin in thyroid cancer.

Table: CPT Codes / HCPCS Codes / ICD-10 Codes
Code Code Description

Information in the [brackets] below has been added for clarification purposes.   Codes requiring a 7th character are represented by "+":

Other CPT codes related to the CPB:

90378 Respiratory syncytial virus, monoclonal antibody, recombinant for intramuscular use, 50 mg each

HCPCS codes covered if selection criteria are met:

Ribavirin (Virazole) Inhalation - no specific code:

ICD-10 codes covered if selection criteria are met:

A92.0 - A92.9 Other mosquito-borne fever (e.g., Rift valley)
A96.2, A98.3 - A98.4
B33.24, B33.8
Other specified diseases due to viruses (e.g., Marburg disease, Tanapox)
A98.0 Crimean-Congo hemorrhagic fever
A98.8 Other specified viral hemorrhagic fevers (e.g., mite-borne hemorrhagic fever)
B33.4 Hantavirus (cardio)-pulmonary syndrome [HPS] [HCPS]
B97.4 Respiratory syncytial virus (RSV) as the cause of diseases classified elsewhere
J21.0 Acute bronchiolitis due to respiratory syncytial virus (RSV)

ICD-10 codes not covered for indications listed in the CPB:

B08.4 Enteroviral vesicular stomatitis with exanthem
B17.2 Acute hepatitis E
C00.0 - C10.9 Malignant neoplasm of lip and oral cavity
C72.0 - C72.9 Malignant neoplasm of central nervous system [glioblastoma]
C73 Malignant neoplasm of thyroid gland
C92.00 - C92.92 Myeloid leukemia
D00.00 - D00.08 Carcinoma in situ of lip, oral cavity, and pharynx
D37.01 - D37.02, D37.04 - D37.09 Neoplasm of uncertain behavior of lip, oral cavity, and pharynx
G35 Multiple sclerosis
J12.2 Parainfluenza virus pneumonia
J20.4 Acute bronchitis due to parainfluenza virus

The above policy is based on the following references:

  1. American Society of Health-System Pharmacists (ASHSP). AHFS Drug Information. Bethesda, MD: ASHSP; updated periodically.
  2. Avery L, Hoffmann C, Whalen Km. The use of aerosolized ribavirin in respiratory syncytial virus lower respiratory tract infections in adult immunocompromised patients: A systematic review. Hosp Pharm. 2020;55(4):224-235.
  3. Beaird OE, Freifeld A, Ison MG, et al. Current practices for treatment of respiratory syncytial virus and other non-influenza respiratory viruses in high-risk patient populations: A survey of institutions in the Midwestern Respiratory Virus Collaborative. Transpl Infect Dis. 2016;18(2):210-215.
  4. Centers for Disease Control and Prevention; Infectious Disease Society of America; American Society of Blood and Marrow Transplantation. Guidelines for preventing opportunistic infections among hematopoietic stem cell transplant recipients. MMWR Recomm Rep. 2000;49(RR-10):1-125, CE1-7.
  5. Choi JH, Jeong K, Kim SM, et al. Synergistic effect of ribavirin and vaccine for protection of early infection stage of foot-and-mouth disease. J Vet Sci. 2018;19(6):788-797.
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  7. Cross JT, Campbell GD. Therapy for nosocomial pneumonia. Med Clin North Am. 2001;85(6):1583-1594.
  8. Dai D, Chen H, Tang J, Tang Y. Inhibition of mTOR/eIF4E by anti-viral drug ribavirin effectively enhances the effects of paclitaxel in oral tongue squamous cell carcinoma. Biochem Biophys Res Commun. 2017;482(4):1259-1264.
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  13. Ison MG. Parainfluenza viruses in adults. UpToDate [online serial], Waltham, MA: UpToDate; reviewed October 2018.
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  19. Ochiai Y, Sano E, Okamoto Y, et al. Efficacy of ribavirin against malignant glioma cell lines: Follow-up study. Oncol Rep. 2018;39(2):537-544.
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  21. Seo S, Xie H, Leisenring WM, et al. Risk factors for parainfluenza virus lower respiratory tract disease after hematopoietic cell transplantation. Biol Blood Marrow Transplant. 2019;25(1):163-171.
  22. Shen X, Zhu Y, Xiao Z, et al. Antiviral drug ribavirin targets thyroid cancer cells by inhibiting the eIF4E-β-catenin axis. Am J Med Sci. 2017;354(2):182-189.
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  24. Smielewska A, Emmott E, Goodfellow I, Jalal H. In vitro sensitivity of human parainfluenza 3 clinical isolates to ribavirin, favipiravir and zanamivir. J Clin Virol. 2018;102:19-26.
  25. Soares-Weiser K, Thomas S, Thomson G, Garner P. Ribavirin for Crimean-Congo hemorrhagic fever: Systematic review and meta-analysis. BMC Infect Dis. 2010;10:207.
  26. Swedish Consensus Group. Management of infections caused by respiratory syncytial virus. Scand J Infect Dis. 2001;33(5):323-328.
  27. Umashanker R, Chopra S. Hepatitis E virus infection. UpToDate [serial online]. Waltham, MA: UpToDate; reviewed October 2014.
  28. Unzueta A, Rakela J. Hepatitis E infection in liver transplant recipients. Liver Transpl. 2014;20(1):15-24.
  29. Ventre K, Randolph AG. Ribavirin for respiratory syncytial virus infection of the lower respiratory tract in infants and young children. Cochrane Database Syst Rev. 2007;(1):CD000181.
  30. Bausch Healthcare US LLC, Virazole (ribavirin for inhalation solution USP). Prescribing Information. REF-VZL-0037. Bridgewater, NJ: Bausch Healthcare US; revised May 2019.
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