Marburg and Ebola — Arming Ourselves against the Deadly Filoviruses

Cj, Peters

doi:10.1056/nejmp058109

Cited by 42 publications

(29 citation statements)

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“…Filoviridae in the order Mononegavirales (MNV), and causes a haemorrhagic fever that is associated with high morbidity and mortality in humans (Peters, 2005). At present, no licensed vaccines or antiviral drugs are available to prevent or treat filoviral diseases.…”

Section: Marburg Virus (Marv) Is a Member Of The Familymentioning

confidence: 99%

Regulation of Marburg virus (MARV) budding by Nedd4.1: a different WW domain of Nedd4.1 is critical for binding to MARV and Ebola virus VP40

Urata

Yasuda

2009

Journal of General Virology

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The VP40 matrix protein of Marburg virus (MARV) has been shown to be the driving force behind MARV budding, a process in which the PPPY L-domain motif of VP40 plays a critical role. Here, we report that Vps4B and Nedd4.1 play critical roles in MARV VP40-mediated budding. We showed that unidentified activities of the Nedd4.1 HECT domain, along with its E3 ubiquitin ligase activity, may be required for MARV budding. Moreover, we showed that the first WW domain of Nedd4.1, WW1, is critical for binding to MARV VP40, indicating that MARV VP40 and Ebola virus VP40 are recognized by a different WW domain of Nedd4.1. This is the first report showing that the viral L-domains containing PPxY have specificities for binding to WW domains. Our findings provide new insights into MARV budding, which may contribute to the development of novel anti-MARV therapeutic strategies.

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Section: Marburg Virus (Marv) Is a Member Of The Familymentioning

confidence: 99%

Regulation of Marburg virus (MARV) budding by Nedd4.1: a different WW domain of Nedd4.1 is critical for binding to MARV and Ebola virus VP40

Urata

Yasuda

2009

Journal of General Virology

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“…An example of a virulence-defeating host-virus interaction is Ebola infection in humans (45). Although Ebola is highly transmissible between humans, it is also highly pathogenic, resulting in almost immediate death of the host.…”

Section: Adaptation and Attenuationmentioning

confidence: 99%

Viral Subversion Mechanisms in Chronic Kidney Disease Pathogenesis

Bruggeman

2007

Clinical Journal of the American Society of Nephrology

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Viruses cannot autonomously replicate but must rely on the host cellular machinery to support their life cycle. Through natural selection, viruses have evolved strategies to co-opt the host organism to be a better site for their propagation. Some of these strategies are directed at the cellular machinery and involve complicated and ingenious solutions to optimize infection, replication, viral gene expression, and new virion assembly and shedding. Other strategies are directed at the host's innate and adaptive immune systems that permit the virus to evade clearance mechanisms. The more common pathogenic viral infections in nephrology-cytomegalovirus, HIV-1, hepatitis C virus, polyomavirus BK, and parvovirus B19 -all have acquired subversion strategies that benefit the virus but because they interfere with normal cellular and immune processes also have become pathogenic to the host. In addition, the highly prevalent viruses cytomegalovirus, BK, and B19 cause severe disease only in the setting of immunosuppression, revealing the very delicate balance that some viruses have achieved with their host's immune system. Thus, selective pressure for survival drives both the evolution of more sophisticated viruses and the host immune system as it evolves to combat the environment of adapting and emerging infectious agents. Understanding the molecular mechanisms of these viral subversion strategies may reveal new targets for the development of highly specific antiviral therapies and also aid vaccine development.

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“…In the last five years, nine outbreaks of filovirus infection have occurred in Uganda, Gabon, Republic of the Congo, Democratic Republic of Congo, and Sudan (Arthur, 2002;Pourrut et al, 2005; http://www.who.int/csr/don/2004_08_07/en/index.html). These include the largest Ebolavirus outbreak yet recorded (425 cases, 83% mortality), centered on Gulu in Uganda in 2000-2001, where initial cases again passed undetected and transmission was amplified within hospitals (WHO, 2001;Okware et al, 2002), the Marburgvirus outbreak around Durba in northeastern Democratic Republic of Congo in 1998-2000, where many of the cases were young men who worked in the local gold mine (the main source of paid employment), and the overall case-fatality rate was 83% (128/154) (WHO, 1999;Bausch et al, 2003), and the 2004-2005 outbreak of Marburgvirus infection in Uige province in Angola (374 cases, 88% mortality), where transmission was amplified by unsafe injections in health care centres, private clinics, and in self-treatment at home (Ndayimirije and Kindhauser, 2005;Peters, 2005; http://www.who.int/csr/don/2005_08_24/en/index.html).…”

Section: Epidemiologymentioning

confidence: 99%

Ebolavirus and Marburgvirus: Insight the Filoviridae family

Ascenzi

Bocedi

Heptonstall

et al. 2008

Molecular Aspects of Medicine

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Ebolavirus and Marburgvirus (belonging to the Filoviridae family) emerged four decades ago and cause epidemics of haemorrhagic fever with high case-fatality rates. The genome of filoviruses encodes seven proteins. No significant homology is observed between filovirus proteins and any known macromolecule. Moreover, Marburgvirus and Ebolavirus show significant differences in protein homology. The natural maintenance cycle of filoviruses is unknown, the natural reservoir, the mode of transmission, the epidemic disease generation, and temporal dynamics are unclear. Lastly, Ebolavirus and Marburgvirus are considered as potential biological weapons. Vaccine appears the unique therapeutic frontier. Here, molecular and clinical aspects of filoviral haemorrhagic fevers are summarized.

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Marburg and Ebola — Arming Ourselves against the Deadly Filoviruses

Cited by 42 publications

References 0 publications

Regulation of Marburg virus (MARV) budding by Nedd4.1: a different WW domain of Nedd4.1 is critical for binding to MARV and Ebola virus VP40

Regulation of Marburg virus (MARV) budding by Nedd4.1: a different WW domain of Nedd4.1 is critical for binding to MARV and Ebola virus VP40

Viral Subversion Mechanisms in Chronic Kidney Disease Pathogenesis

Ebolavirus and Marburgvirus: Insight the Filoviridae family

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