Healthcare-associated exposure to Borna disease virus 1 (BoDV-1)

Abstract

The Borna disease virus 1 (BoDV-1) causes severe and often fatal encephalitis in humans. The virus is endemic in parts of Germany, Liechtenstein, Switzerland and Austria. As an increasing number of human BoDV-1 encephalitis cases is being diagnosed, the chance for healthcare professionals to come into contact with infected tissues and bodily fluids from patients with known acute bornavirus encephalitis is also increasing. Therefore, risk assessments are needed. Based on three different incidences of possible exposure to BoDV-1 including an autopsy knife injury, a needlestick injury, and a spill accident with cerebrospinal fluid from patients with acute BoDV-1 encephalitis, we perform risk assessments and review published data. BoDV-1 infection status of the index patient's tissues and bodily fluids to which contact had occurred should be determined. There is only scarce evidence for possible postexposure prophylaxis, serology, and imaging in healthcare professionals who possibly came into contact with the virus. Despite decade-long laboratory work with BoDV-1, not a single clinically apparent laboratory infection has been published. Given the increasing number of severe or fatal BoDV-1 encephalitis cases, there is a growing need for efficacy-tested, potent antiviral therapeutics against BoDV-1 in humans, both in clinically ill patients and possibly as postexposure prophylaxis in healthcare professionals.

Keywords: Bornavirus; Favipiravir; Imaging; Postexposure prophylaxis; Serology.

Fig. 1

BoDV-1 detection in a peripheral nerve. Positive immunostaining for BoDV-1 phosphoprotein in peripheral nerve surrounding hepatoduodenal lymph nodes – index patient, scenario 1. Scale bar: 50 μm

Fig. 2

Schematic drawing of postexposure procedures discussed in the text. After a possible exposure, immediate wound care should be performed, followed by gathering information about the bornavirus status of the index patient, the type of accident, and to which possibly virus contaminated material the contact patient was exposed. Further options, such as serology, imaging and the question of a possible postexposure prophylaxis may be considered depending on the individual scenario

Fig. 3

Typical cranial magnetic resonance imaging of early BoDV-1 encephalitis. Left column: T2 weighted imaging (top left) shows discrete, nearly symmetric hyperintensities of the insular ribbon (IR), the posteromedial thalamus (PMT), the caudate head (CH) and the lentiform nucleus (LN). These changes are more easily appreciated on diffusion-weighted imaging (DWI, bottom left), where diffusion restriction in these brain areas is visualized as a hyperintense signal. Right column: T2 weighted imaging (top right) shows progressive T2 hyperintensities of the affected areas with associated parenchymal swelling, somewhat more pronounced on the patient’s left side. No T1 hyperintense signal changes, which are characteristic of late-stage BoDV-1 encephalitis, were present at this time point (bottom right)