Biology Essays - VHF Viruses


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VHF Viruses and Viral Hemorrhagic Fevers

An outbreak ofEbola virus in Zaire in May 1995 first focused international attention on thegroup of diseases known collectively as viral hemorrhagic fevers (VHFs) (Tolan,2004). These fever and bleeding disorders affect multiple organ systems, with severity varyingwidely from comparatively mild illness to fatal disease (Centers for DiseaseControl and Prevention (CDC), 2004). The causal agents in VHF are a diversegroup of lipid-enveloped, zoonotic, RNA viruses, each of which can be groupedinto one of four distinct families - filoviruses, arenaviruses, bunyavirusesand flaviviruses (Center for Biosecurity, 2004).


The natural reservoirfor VHF viruses is animal hosts, primarily rodents or arthropod vectors such asticks and mosquitoes. Human infection results from contact with a contaminatedhost - e.g. an arthropod bite, direct handling of animal carcasses orinhalation of the aerosol from infected rodent excrement (LeDuc, 1989). Onceinfected, inter-human transmission of most VHF viruses is possible via closecontact with the infected patient, their bodily fluids and/or contaminateditems such as syringes (Tolan, 2004; Center for Biosecurity, 2004). Airborne transmissibilityhas not been conclusively established, although transfer via this route appearsrare (Borio et al, 2002).


Following a 2-12day incubation period, VHF presents with initial non-specific symptoms such as markedfever, myalgia, malaise, arthralgia, fatigue, headache and weakness. Bleeding manifestationsoften occur in severe disease or as the infection progresses, with patientsshowing subcutaneous, internal or orificial bleeding - although this hemorrhagingis rarely fatal. Severe cases of VHF are associated with hypotension and shock,pneumonitis, pleural and pericardial effusion, encephalopathy, seizure, comaand often, death (Tolan, 2004; CDC, 2004).

VHF virusfamilies


The filoviruses,Marburg and Ebola, are filamentous in nature and comprised of a 19 kb non-segmentedRNA genome (Feldman & Klenk, 1996). Both filoviruses elicit clinicallysimilar signs and symptoms - including development of a morbilliform rash onaround day five of the disease (Tolan, 2004). Although Ebola, for which four distinctsubtypes - Zaire, Sudan, Reston and Ivory Coast- have been identified, causesmore severe disease than Marburg (Feldman & Klenk, 1996; Tolan, 2004; Borioet al, 2002). Multiple hemorrhages, extensive hepatic involvement anddisseminated intravascular coagulation leading to a septic shock-type syndrome arefeatures of filovirus infection (Feldman & Klenk, 1996; Tolan, 2004). Mortalityrates are significant, ranging from 30 to 90%, with VHF typically proving fatal6-16 days after filovirus infection. The pathogenic mechanisms underlying theseviruses are complex and appear to include widespread cellular effects,immunosuppression and induction of significant inflammatory responses (Feldman& Klenk, 1996; Mahanty & Bray, 2004).

In total,approximately 18 human outbreaks of filovirus-related VHF have been reported,equating to 1500 cases, all stemming from African origin. Thus far, noviral vector has been pinpointed. Direct physical contact with an infectedperson is the primary transmission route (Feldman & Klenk, 1996; Schou, 2000).


Bunyaviruses arespherical viruses which include Crimean Congo hemorrhagic fever (CCHF) virus,Rift Valley fever (RVF) virus and the Hanta viruses. Manifesting clinically asfever with rash, bunyavirus infection is also associated with hemorrhage, whichis characteristically severe in CCHF. RVF elicits retinal vasculitis which canlead to permanent blindness. The precise pathogenic mechanism in bunyavirusinfection is unclear - viremia follows the incubation period which lasts a fewdays (Shope, 1996; Tolan, 2004; Center for Biosecurity, 2004).

Excluding thehantaviruses which reside in rodent hosts, bunyaviruses are transmitted viaarthropod vector - tick, mosquito, midge or sand fly.


Five arenavirusesproduce disease in humans including the Lassa fever virus, three Latin Americanviral strains and lymphocytic choriomeningitis (LCM) virus. Struturally, thearenavirus appears round, oval or can be pleomorphic. Infection with four ofthe five virus types, including Lassa, induces similar clinical signs andsymptoms which include fever and malaise. However, where Latin American viralinfection has greater propensity for progression to hemorrhaging andneurological and cellular effects, Lassa is more commonly associated withhepatitis. In contrast, 70% of LCM virus infections are asymptomatic ormanifest as nothing more severe than a common influenza/gastrointestinalinfection (Pfau, 1996).

Arenaviruses are non-pathogenicin their rodent vector hosts and transmitted to humans via contact with infectedfeces or urine. Pathogenesis in humans is unclear, as is the precise mechanismof viral entry (Pfau, 1996).


Sphericalflaviviruses are causative agents for VHFs encompassing dengue, yellow fever,Omsk hemorrhagic fever and Kyasanur Forest virus disease. The viruses arespread in the saliva of infected arthropod hosts, namely mosquitoes and ticks,with viremia occurring after viral release from lysing, infected cells. Theflaviviruses can be categorized into three groups based on their underlyingdisease mechanisms and primary association with the clinical manifestation of:

  • encephalitis
  • arthralgia, fever and rash (e.g. dengue)
  • hemorrhagic fever (e.g. Kyasanur Forest virus disease)
  • hemorrhagic fever with accompanying hepatitis (yellow fever) (Schmaljohn & McClain, 1996).


Currently, noanti-viral therapy exists to treat VHF and there is no effective cure. Theanti-hepatitis agent, ribavarin, has shown activity against certainbunyaviruses and arenaviruses, particularly Lassa fever. Vaccines are availablefor yellow fever and Argentine hemorrhagic fever only (CDC, 2004; Center forBiosecurity, 2004).

Prompt diagnosisand supportive therapy are key to reducing mortality in VHF. The cornerstone ofcurrent therapy is simple management with fluids and electrolytes (Tolan, 2004).Many VHFs are classified as biosafety level four (BSL-4) viruses which must be handledunder high containment (CDC, 2004).


VHF is foundaround the globe, but restricted mainly to sites of host/vector population.However, increasing international travel is shifting the natural picture of VHFdistribution - with these diseases now beginning to appear in new andunfamiliar Western territories (CDC, 2004). Given the deficiency of effectiveprophylaxis and treatment, coupled with the virulent nature of these diseases,VHF is likely to remain the subject of scientific investigation and endeavorfor many years to come.


Borio, L.,Inglesby, T., Peters, C., 2002. Hemorrhagic fever viruses as biological weapons.Journal of the American Medical Association, 287(18), 2391-2405.

Center forBiosecurity, 2004. Viral hemorrhagic fevers fact sheet, University ofPittsburgh Medical Center. Available from:[Accessed 17 February 2005].

Centers forDisease Control and Prevention (CDC), 2004. Viral hemorrhagic fevers factsheet, Special Pathogens Branch. Available from:[Accessed 17 February 2005].

Feldman, H. &Klenk, H-D., 1996. Filoviruses. In: S. Baron, ed. Medicalmicrobiology. Glaveston, TX: University of Texas Medical Branch, chapter 72.

LeDuc, J., 1989.Epidemiology of hemorrhagic fever viruses. Rev Infect Dis, 11(suppl 4),S730-735.

Levinson, W. &Jawetz, E., 1998. Examination & board review: Medical microbiology &immunology. 5th ed. Stamford, CT: Appleton & Lange.

Mahanty, S. &Bray, M., 2004. Pathogenesis of filoviral hemorrhagic fevers. Lancet InfectDis, 4(8), 487-498.

Pfau, C., 1996.Arenaviruses. In: S. Baron, ed. Medical microbiology. Glaveston, TX:University of Texas Medical Branch, chapter 57.

Schmaljohn, A.& McClain, D., 1996. Alphaviruses (togaviridae) and flaviviruses(flaviviridae). In: S. Baron, ed. Medical microbiology. Glaveston, TX:University of Texas Medical Branch, chapter 54.

Schou, S., Hansen,A., 2000. Marburg and Ebola virus infection in laboratory nonhuman primates: aliterature review. Comp Med, 50, 108-123.

Shope, R., 1996.Bunyaviruses. In: S. Baron, ed. Medical microbiology. Glaveston, TX:University of Texas Medical Branch, chapter 56.

Tolan, R., 2004. Viralhemorrhagic fevers. Emedicine. Available from:[Accessed 17 February 2005].

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