Inhibition of Crimean-Congo Hemorrhagic Fever Viral Infectivity Yields in Vitro by Ribavirin

Watts, Douglas M.; Ussery, Michael A.; Nash, Denise; Peters, C. J.

doi:10.4269/ajtmh.1989.41.581

Cited by 114 publications

(77 citation statements)

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“…Inhibition of CCHFV replication has been demonstrated in a minigenome system (Bergeron et al, 2010), in virus-infected cells (Huggins, 1989;Watts et al, 1989;Paragas et al, 2004), in newborn mice (Tignor and Hanham, 1993) and in STAT-1 KO mice (Bente et al, 2010). Comparisons of a number of virus strains found that they differed no more than a few-fold in sensitivity to the drug Paragas et al, 2004).…”

Section: Ribavirinmentioning

confidence: 99%

“…In cells that lack SKI-1, PreG N and PreG C accumulate in the Golgi apparatus, and infected cells secrete virus particles lacking surface glycoproteins (Bergeron et al, 2007). (Papa et al (2002c(Papa et al ( ) 1948(Papa et al ( -2000 Khazakhstan 108 35 Hoogstraal (1979) and Yashina et al (2003Yashina et al ( ) 1943Yashina et al ( -2010 Tajikistan 237 16 Asia-2 IV; M2 Hoogstraal (1979), Seregin et al (2004) and Ergonul (2010Ergonul ( ) 1976Ergonul ( -2000 Pakistan 23 39 Asia-1 IV; M1; M2; Asia-IV Burney et al (1980) and Smego et al (2004Smego et al ( ) 2011 India 6 83 Asia-2 IV; M2; Asia-IV Yadav et al (2013) Suleiman et al (1980), Schwarz et al (1997) and Watts et al (1989Watts et al ( ) 1990 Saudi Arabia 7 0 El-Azazy and Scrimgeour (1997Scrimgeour ( ) 1995Scrimgeour ( -1997 Oman 4 Asia-1 IV; M1; Asia-IV Saluzzo et al (1985Saluzzo et al ( ) 1979Saluzzo et al ( -1980 Iraq 55 Saluzzo et al (1985) and Nabeth et al (2004aNabeth et al ( , 2004bNabeth et al ( ) 1983 Burkina Faso 1 0 Watts et al (1989Watts et al ( ) 1981Watts et al ( -1986 South Africa 32 31 S Africa/W Africa-III; M1; M2 Watts et al (1989) Elata et al (2011) N-linked glycosylation of G N is also essential for the final processing of both glycoproteins (Erickson et al, 2007). G N performs a chaperone-like function for G C , and must be present for correct folding to occur (Shi et al, 2012).…”

Section: The M Segmentmentioning

confidence: 99%

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Crimean-Congo hemorrhagic fever: History, epidemiology, pathogenesis, clinical syndrome and genetic diversity

et al. 2013

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Bente, Dennis A.; Forrester, Naomi L.; Watts, Douglas M.; McAuley, Alexander J.; Whitehouse, Chris A.; and Bray, Mike, "CrimeanCongo hemorrhagic fever: History, epidemiology, pathogenesis, clinical syndrome and genetic diversity" (2013 b s t r a c tCrimean-Congo hemorrhagic fever (CCHF) is the most important tick-borne viral disease of humans, causing sporadic cases or outbreaks of severe illness across a huge geographic area, from western China to the Middle East and southeastern Europe and throughout most of Africa. CCHFV is maintained in vertical and horizontal transmission cycles involving ixodid ticks and a variety of wild and domestic vertebrates, which do not show signs of illness. The virus circulates in a number of tick genera, but Hyalomma ticks are the principal source of human infection, probably because both immature and adult forms actively seek hosts for the blood meals required at each stage of maturation. CCHF occurs most frequently among agricultural workers following the bite of an infected tick, and to a lesser extent among slaughterhouse workers exposed to the blood and tissues of infected livestock and medical personnel through contact with the body fluids of infected patients. CCHFV is the most genetically diverse of the arboviruses, with nucleotide sequence differences among isolates ranging from 20% for the viral S segment to 31% for the M segment. Viruses with diverse sequences can be found within the same geographic area, while closely related viruses have been isolated in far distant regions, suggesting that widespread dispersion of CCHFV has occurred at times in the past, possibly by ticks carried on migratory birds or through the international livestock trade. Reassortment among genome segments during co-infection of ticks or vertebrates appears to have played an important role in generating diversity, and represents a potential future source of novel viruses. In this article, we first review current knowledge of CCHFV, summarizing its molecular biology, maintenance and transmission, epidemiology and geographic range. We also include an extensive discussion of CCHFV genetic diversity, including maps of the range of the virus with superimposed phylogenetic trees. We then review the features of CCHF, including the clinical syndrome, diagnosis, treatment, pathogenesis, vaccine development and laboratory animal models of CCHF. The paper ends with a discussion of the possible future geographic range of the virus. For the benefit of researchers, we include a Supplementary Table listing all published reports of CCHF cases and outbreaks in the English-language literature, plus some principal articles in other languages, with total case numbers, case fatality rates and all CCHFV strains on GenBank.

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Section: Ribavirinmentioning

confidence: 99%

Section: The M Segmentmentioning

confidence: 99%

Crimean-Congo hemorrhagic fever: History, epidemiology, pathogenesis, clinical syndrome and genetic diversity

et al. 2013

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“…During the 2000 Saudi Arabia outbreak, a small clinical trial evaluating the effectiveness of ribavirin to treat severe RVFV infection suggested an increase in the incidence of encephalitis in ribavirin-treated cases; however, these results are inconclusive (P. Rollin, presented at the Treatment of Viral Hemorrhagic Fever Workshop, Bethesda, MD, February 24 to 27,2007). Ribavirin has proven effective against CCHFV in cell culture, mice, 10,11 and several …”

Section: Discussionmentioning

confidence: 99%

“…Ribavirin, a nucleoside analog, has antiviral activity against the hantaviruses, phleboviruses, nairoviruses, and the orthobunyaviruses. [4][5][6][7][8][9][10][11][12][13][14][15][16] While ribavirin has proven to be effective and is generally the standard other antiviral compounds are measured against, it is not without its limitations. First, there are concerns about its side-effects such as hemolytic anemia and potential teratogenicity.…”

Section: Introductionmentioning

confidence: 99%

Development of FGI-106 as a broad-spectrum therapeutic with activity against members of the family Bunyaviridae

Kinch¹

2010

VAAT

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Virus Adaptation and Treatment Abstract:The family Bunyaviridae is a diverse group of negative-strand RNA viruses that infect a wide range of arthropod vectors and animal hosts. Based on the continuing need for new therapeutics to treat bunyavirus infections, we evaluated the potential efficacy of FGI-106, a small-molecular compound that previously demonstrated activity against different RNA viruses. FGI-106 displayed substantial antiviral activity in cell-based assays of different bunyavirus family members, including Asian and South American hantaviruses (Hantaan virus and Andes virus), Crimean-Congo hemorrhagic fever virus, La Crosse virus, and Rift Valley fever virus. The pharmacokinetic profile of FGI-106 revealed sufficient exposure of the drug to critical target organs (lung, liver, kidney, and spleen), which are frequently the sites of bunyavirus replication. Consistent with these findings, FGI-106 treatment delivered via intraperitoneal injection prior to virus exposure was sufficient to delay the onset of Rift Valley fever virus infection in mouse-based models and to enhance survival in the face of an otherwise lethal infection. Altogether, these results suggest a potential opportunity for the use of FGI-106 to treat infections by members of the family Bunyaviridae.

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“…22 Ribavirin treatment was administered to 46 cases (43 non fatal-three fatal cases). The efficacy of ribavirin in the treatment of CCHF is not clear.…”

Section: Discussionmentioning

confidence: 99%

Crimean-Congo Hemorrhagic Fever Virus Infection: Clinical and Laboratory Observations and Predictors of Fatality

Kadanalı¹,

Özden²,

Erol³

2012

Turkiye Klinikleri J Med Sci

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A AB BS ST TR RA AC CT T O Ob bj je ec ct ti iv ve e: : In this study we described the predictors of fatality among Crimean-Congo hemorrhagic fever (CCHF) patients who admitted to our hospital based on epidemiological, clinical and laboratory findings between 2005 and 2006. M Ma at te er ri ia al l a an nd d M Me et th ho od ds s: : Definitive diagnosis was based on the detection of CCHF virus-specific IgM by ELISA and/or of genomic segments of the CCHF virus by real time polymerase chain reaction. Related data were collected prospectively. R Re es su ul lt ts s: : The study included 63 patients. Thirty-two of the patients (50.8%) were females and 31 of them (49.2%) were males. The overall case fatality rate was 4.8 %. The age and sex were similar between favorable and fatal cases (p>0.05). The mean duration to the onset of symptoms for all patients was 4.7 days and differences in the mean duration to the onset of symptoms between surviving and died patients were not statistically significant (p=0.22). Weakness, myalgia, somnolence, bleeding from multiple sites and presence of petechia/ecchymosis were observed more often in the patients who died (p=0.02, p=0.03, p=0.015, p=0.02, respectively). Significant elevation of LDH levels (p=0.004), prolonged APT (p=0.004), prolonged PT (p=0.04) and thrombocytopenia (p=0.01) were detected in patients who died. Oral ribavirin was prescribed to 46 patients (73%). Prescription of ribavirin was considered to three patients with fatal disease, but this could not be realized because of hematemesis and melena. C Co on nc cl lu us si io on n: : The existence of various clinical and laboratory findings like weakness, myalgia, somnolence, bleeding, elevation of LDH levels, prolonged APT and PT and thrombocytopenia may be considered as risk factors for fatality in CCHF. İyi olgularla ölümcül olgular arasında yaş ve cinsiyet benzerdi (p>0,05). Tüm hastalarda belirtiler ortaya çıkana kadar geçen ortalama süre 4,7 gündü ve hayatta kalan ve ölen hastalar arasında belirtiler ortaya çıkana kadar geçen süre bakımından istatistiksel olarak anlamlı fark yoktu (p=0,22). Güçsüzlük, myalji, uyku hali, birden fazla bölgeden kanama ve peteşi/ekimoz varlığı ölen hastalarda daha sık gözlendi (p=0,02, p=0,03, p=0,015, p=0,02). Ölen hastalarda LDH düzeylerinde önemli yük-selme (p=0,004), uzamış APT (p=0,004), uzamış PT (p=0,04) ve trombositopeni (p=0,01) saptandı. Kırkaltı hastada (%73) oral ribavirin verildi. Fatal üç hastaya ribavirin verilmesi düşünüldü fakat hematemez ve melena nedeniyle gerçekleştirilemedi. S So on nu uç ç: : Güçsüzlük, myalji, uyku hali, kanama, LDH düzeylerinde yükselme, uzamış APT ve PT, trombositopeni gibi çeşitli klinik ve laboratuvar bulgularının varlığı KKKA'da fatalite için risk faktörleri olarak düşünülebilir.A An na ah ht ta ar r K Ke el li im me el le er r: : Hemorajik ateş virüsü, kırım-kongo; tanı; keneler T Tu ur rk ki iy ye e K Kl li in ni ik kl le er ri i J J M Me ed d S Sc ci i 2 20 01 12 2; ;3 32 2( (2 2) ): :4 43 32 2--7 7

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Inhibition of Crimean-Congo Hemorrhagic Fever Viral Infectivity Yields in Vitro by Ribavirin

Cited by 114 publications

References 0 publications

Crimean-Congo hemorrhagic fever: History, epidemiology, pathogenesis, clinical syndrome and genetic diversity

Crimean-Congo hemorrhagic fever: History, epidemiology, pathogenesis, clinical syndrome and genetic diversity

Development of FGI-106 as a broad-spectrum therapeutic with activity against members of the family Bunyaviridae

Crimean-Congo Hemorrhagic Fever Virus Infection: Clinical and Laboratory Observations and Predictors of Fatality

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