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Pathogen Page

Marburg Virus

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Hemorrhagic fever

3. Introduction

Marburg was identified in 1967 in Central Africa. It has been known to infect bats, humans, and non-human primates. The virus has caused severe outbreaks of, usually, fatal hemorrhagic fever. In primates, the symtoms are known to be fever, diarrhea, vomiting, coagulation deficits, and severe liver damage. The virus causes a profuse release of inflammatory cytokines, which affects vascular permeability. The excessive bleeding involved sometimes leads to the activation of tissue factor in macrophages and monocytes, as well as a drop in platlet numbers (Mohamadzadeh et al., 2007).

4. Microbial Pathogenesis

The initial targets of infection are generally macrophages, monocytes, and DCs. Filoviruses generally bind to the TREM or C-type lectin receptors on myloid cells. However, since some cells do not express C-lectin or TREM receptors, viral entry may be due to molecules such as heparin-sulphate proteoglycan and folate receptor-α. Data also indicate that the expression of TLR1 (whose signal converges with that of TLR2) was increased on MARV-activated neutrophils (Mohamadzadeh et al., 2007).

5. Host Ranges and Animal Models

The natural host for MARV is known to be bats of Central African origin (Mohamadzadeh et al., 2007).

6. Host Protective Immunity

Filoviruses have been found to disable some of the host IFN pathway, such as the VP35, which prevents the production of type I IFNs, and VP24, which interferes with the abilities of certain molecules to induce antiviral states. IFN is crucial to immune response, as indicated by elevated levels of IFN in the blood even during acute infection. It had also been seen that there is a deficit (virus-induced) in the co-stimulatory properties of infected Dcs, identified by a supressed capacity of the DCs to stimulate allogenic T cells. By affecting either viral exit or entry, cellular proteases could influence viral cellular tropisms and interactions between antibodies and glycoproteins. All host protective immunity observations are also tied with the prevalence of an abundance of cathepsins (Mohamadzadeh et al., 2007).

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