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Free Essays - Biology Essays

VHF Viruses and Viral Hemorrhagic Fevers

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

Transmission

The natural reservoir for VHF viruses is animal hosts, primarily rodents or arthropod vectors such as ticks and mosquitoes. Human infection results from contact with a contaminated host - e.g. an arthropod bite, direct handling of animal carcasses or inhalation of the aerosol from infected rodent excrement (LeDuc, 1989). Once infected, inter-human transmission of most VHF viruses is possible via close contact with the infected patient, their bodily fluids and/or contaminated items such as syringes (Tolan, 2004; Center for Biosecurity, 2004). Airborne transmissibility has not been conclusively established, although transfer via this route appears rare (Borio et al, 2002).

Clinical manifestation

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

VHF virus families

Filoviruses

The filoviruses, Marburg and Ebola, are filamentous in nature and comprised of a 19 kb non-segmented RNA genome (Feldman & Klenk, 1996). Both filoviruses elicit clinically similar signs and symptoms - including development of a morbilliform rash on around day five of the disease (Tolan, 2004). Although Ebola, for which four distinct subtypes - Zaire, Sudan, Reston and Ivory Coast- have been identified, causes more severe disease than Marburg (Feldman & Klenk, 1996; Tolan, 2004; Borio et al, 2002). Multiple hemorrhages, extensive hepatic involvement and disseminated intravascular coagulation leading to a septic shock-type syndrome are features of filovirus infection (Feldman & Klenk, 1996; Tolan, 2004). Mortality rates are significant, ranging from 30 to 90%, with VHF typically proving fatal 6-16 days after filovirus infection. The pathogenic mechanisms underlying these viruses 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, no viral vector has been pinpointed. Direct physical contact with an infected person is the primary transmission route (Feldman & Klenk, 1996; Schou, 2000).

Bunyaviruses

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

Excluding the hantaviruses which reside in rodent hosts, bunyaviruses are transmitted via arthropod vector - tick, mosquito, midge or sand fly.

Arenaviruses

Five arenaviruses produce disease in humans including the Lassa fever virus, three Latin American viral strains and lymphocytic choriomeningitis (LCM) virus. Struturally, the arenavirus appears round, oval or can be pleomorphic. Infection with four of the five virus types, including Lassa, induces similar clinical signs and symptoms which include fever and malaise. However, where Latin American viral infection has greater propensity for progression to hemorrhaging and neurological and cellular effects, Lassa is more commonly associated with hepatitis. In contrast, 70% of LCM virus infections are asymptomatic or manifest as nothing more severe than a common influenza/gastrointestinal infection (Pfau, 1996).

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

Flaviviruses

Spherical flaviviruses are causative agents for VHFs encompassing dengue, yellow fever, Omsk hemorrhagic fever and Kyasanur Forest virus disease. The viruses are spread in the saliva of infected arthropod hosts, namely mosquitoes and ticks, with viremia occurring after viral release from lysing, infected cells. The flaviviruses can be categorized into three groups based on their underlying disease 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).

Treatments

Currently, no anti-viral therapy exists to treat VHF and there is no effective cure. The anti-hepatitis agent, ribavarin, has shown activity against certain bunyaviruses and arenaviruses, particularly Lassa fever. Vaccines are available for yellow fever and Argentine hemorrhagic fever only (CDC, 2004; Center for Biosecurity, 2004).

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

Conclusion

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

References

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

Center for Biosecurity, 2004. Viral hemorrhagic fevers fact sheet, University of Pittsburgh Medical Center. Available from: http://www.upmc-biosecurity.org/print/pages/agents/p_vhf.html [Accessed 17 February 2005].

Centers for Disease Control and Prevention (CDC), 2004. Viral hemorrhagic fevers fact sheet, Special Pathogens Branch. Available from: http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/vhf.htm [Accessed 17 February 2005].

Feldman, H. & Klenk, H-D., 1996. Filoviruses. In: S. Baron, ed. Medical microbiology. 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. 5^th ed. Stamford, CT: Appleton & Lange.

Mahanty, S. & Bray, M., 2004. Pathogenesis of filoviral hemorrhagic fevers. Lancet Infect Dis, 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: a literature 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. Viral hemorrhagic fevers. Emedicine. Available from: http://www.emedicine.com/ped/topic2406.htm [Accessed 17 February 2005].

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