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      Hendra and Nipah Virus Infection in Cultured Human Olfactory Epithelial Cells

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          Abstract

          Henipaviruses are emerging zoonotic pathogens that can cause acute and severe respiratory and neurological disease in humans. The pathways by which henipaviruses enter the central nervous system (CNS) in humans are still unknown. The observation that human olfactory neurons are highly susceptible to infection with henipaviruses demonstrates that the olfactory epithelium can serve as a site of Henipavirus entry into the CNS.

          ABSTRACT

          Henipaviruses are emerging zoonotic viruses and causative agents of encephalitis in humans. However, the mechanisms of entry into the central nervous system (CNS) in humans are not known. Here, we evaluated the possible role of olfactory epithelium in virus entry into the CNS. We characterized Hendra virus (HeV) and Nipah virus (NiV) infection of primary human olfactory epithelial cultures. We show that henipaviruses can infect mature olfactory sensory neurons. Henipaviruses replicated efficiently, resulting in cytopathic effect and limited induction of host responses. These results show that human olfactory epithelium is susceptible to infection with henipaviruses, suggesting that this could be a pathway for neuroinvasion in humans.

          IMPORTANCE Henipaviruses are emerging zoonotic pathogens that can cause acute and severe respiratory and neurological disease in humans. The pathways by which henipaviruses enter the central nervous system (CNS) in humans are still unknown. The observation that human olfactory neurons are highly susceptible to infection with henipaviruses demonstrates that the olfactory epithelium can serve as a site of Henipavirus entry into the CNS.

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          Clinical features of Nipah virus encephalitis among pig farmers in Malaysia.

          S A Sarji, David Tan, Thean Chew … (2000)
          Between September 1998 and June 1999, there was an outbreak of severe viral encephalitis due to Nipah virus, a newly discovered paramyxovirus, in Malaysia. We studied the clinical features of the patients with Nipah virus encephalitis who were admitted to a medical center in Kuala Lumpur. The case definition was based on epidemiologic, clinical, cerebrospinal fluid, and neuroimaging findings. Ninety-four patients with Nipah virus infection were seen from February to June 1999 (mean age, 37 years; ratio of male patients to female patients, 4.5 to 1). Ninety-three percent had had direct contact with pigs, usually in the two weeks before the onset of illness, suggesting that there was direct viral transmission from pigs to humans and a short incubation period. The main presenting features were fever, headache, dizziness, and vomiting. Fifty-two patients (55 percent) had a reduced level of consciousness and prominent brain-stem dysfunction. Distinctive clinical signs included segmental myoclonus, areflexia and hypotonia, hypertension, and tachycardia and thus suggest the involvement of the brain stem and the upper cervical spinal cord. The initial cerebrospinal fluid findings were abnormal in 75 percent of patients. Antibodies against Hendra virus were detected in serum or cerebrospinal fluid in 76 percent of 83 patients tested. Thirty patients (32 percent) died after rapid deterioration in their condition. An abnormal doll's-eye reflex and tachycardia were factors associated with a poor prognosis. Death was probably due to severe brain-stem involvement. Neurologic relapse occurred after initially mild disease in three patients. Fifty patients (53 percent) recovered fully, and 14 (15 percent) had persistent neurologic deficits. Nipah virus causes a severe, rapidly progressive encephalitis with a high mortality rate and features that suggest involvement of the brain stem. The infection is associated with recent contact with pigs.
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            Clinical presentation of nipah virus infection in Bangladesh.

            Emily S. Gurley, Robert Breiman, P Formenty … (2008)
            In Bangladesh, 4 outbreaks of Nipah virus infection were identified during the period 2001-2004. We characterized the clinical features of Nipah virus-infected individuals affected by these outbreaks. We classified patients as having confirmed cases of Nipah virus infection if they had antibodies reactive with Nipah virus antigen. Patients were considered to have probable cases of Nipah virus infection if they had symptoms consistent with Nipah virus infection during the same time and in the same community as patients with confirmed cases. We identified 92 patients with Nipah virus infection, 67 (73%) of whom died. Although all age groups were affected, 2 outbreaks principally affected young persons (median age, 12 years); 62% of the affected persons were male. Fever, altered mental status, headache, cough, respiratory difficulty, vomiting, and convulsions were the most common signs and symptoms; clinical and radiographic features of acute respiratory distress syndrome of Nipah illness were identified during the fourth outbreak. Among those who died, death occurred a median of 6 days (range, 2-36 days) after the onset of illness. Patients who died were more likely than survivors to have a temperature >37.8 degrees C, altered mental status, difficulty breathing, and abnormal plantar reflexes. Among patients with Nipah virus infection who had well-defined exposure to another patient infected with Nipah virus, the median incubation period was 9 days (range, 6-11 days). Nipah virus infection produced rapidly progressive severe illness affecting the central nervous and respiratory systems. Clinical characteristics of Nipah virus infection in Bangladesh, including a severe respiratory component, appear distinct from clinical characteristics reported during earlier outbreaks in other countries.
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              Infection of humans and horses by a newly described morbillivirus.

              Kevin J. Sheridan, Graham K. Murray, A Ansford … (1995)
              To describe the clinical and epidemiological features of an outbreak of a viral infection affecting humans and horses. Stables in Hendra, a suburb of Brisbane. Affected horses and humans, and at-risk human contacts. A pregnant mare died two days after arrival from a paddock elsewhere in Brisbane. Eight to 11 days later, illness (depression, anorexia, fever, dyspnoea, ataxia, tachycardia, tachypnoea and nasal discharge) was reported among 17 other horses from the same or an adjoining stable. Fourteen horses died or were put down. Five and six days after the index mare's death, a stable-hand and then a horse-trainer, both of whom had had close contact with the sick mare's mucous secretions, developed influenza-like illnesses. The stable-hand recovered but the trainer developed pneumonitis, respiratory failure, renal failure and arterial thrombosis, and died from a cardiac arrest seven days after admission to hospital. A morbillivirus cultured from his kidney was identical to one isolated from the lungs of five affected horses. The two affected humans and eight other horses were seropositive for the infection, which was reproduced in healthy horses following challenge by spleen/lung homogenates from infected horses. There was no serological evidence of infection in 157 humans who had had contact with the stables or the sick horses or humans. A previously undescribed morbillivirus infected a probable 21 horses and two humans; one human and 14 horses died. That no further cases were detected among humans suggests that the virus was of low infectivity. The source of infection remains undetermined.
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                Author and article information

                Contributors
                Benhur Lee: Role: Editor
                Journal
                Journal ID (nlm-ta): mSphere
                Journal ID (iso-abbrev): mSphere
                Journal ID (hwp): msph
                Journal ID (pmc): msph
                Journal ID (publisher-id): mSphere
                Title: mSphere
                Publisher: American Society for Microbiology (1752 N St., N.W., Washington, DC )
                ISSN (Electronic): 2379-5042
                Publication date (Electronic): 28 June 2017
                Publication date Collection: May-Jun 2017
                Volume: 2
                Issue: 3
                Electronic Location Identifier: e00252-17
                Affiliations
                [a ]Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA
                [b ]Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA
                [c ]Monell Chemical Senses Center, Philadelphia, Pennsylvania, USA
                [d ]Department of Viroscience, Erasmus University Medical Centre, Rotterdam, The Netherlands
                Icahn School of Medicine at Mount Sinai
                Author notes
                Address correspondence to Barry Rockx, b.rockx@ 123456erasmusmc.nl .

                V.B. and M.H.O. contributed equally to this work.

                Citation Borisevich V, Ozdener MH, Malik B, Rockx B. 2017. Hendra and Nipah virus infection in cultured human olfactory epithelial cells. mSphere 2:e00252-17. https://doi.org/10.1128/mSphere.00252-17.

                Article
                Publisher ID: mSphere00252-17
                DOI: 10.1128/mSphere.00252-17
                PMC ID: 5489660
                SO-VID: 1743fb4e-d236-4a5a-83e0-b556da0f6656
                Copyright © Copyright © 2017 Borisevich et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.

                History
                Date received : 2 June 2017
                Date accepted : 8 June 2017
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 22, Pages: 5, Words: 2613
                Categories
                Subject: Observation
                Subject: Host-Microbe Biology
                Custom metadata
                cover-date May/June 2017

                Keywords: henipavirus,neuroinvasion,olfactory epithelium
                Data availability:
                Keywords: henipavirus, neuroinvasion, olfactory epithelium

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