Molecular Interactions in the Assembly of Coronaviruses

Haan, Cornelis A. M. de; Rottier, Peter J. M.

doi:10.1016/s0065-3527(05)64006-7

Cited by 356 publications

(360 citation statements)

References 289 publications

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“…We did not observe surface localization of TSG101 in human embryonic lung L-132 cells infected with human coronavirus-229E or simian kidney MA104 cells infected with simian rotavirus SA11-4F (data not shown). Neither of the viruses buds from the cell membrane, 26,27 which is consistent with the absence of TSG101 surface exposure.…”

Section: Discussionsupporting

confidence: 73%

Antibody targeting of TSG101 on influenza-infected cells

Kinch¹

2010

VAAT

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Influenza remains a significant cause of morbidity and mortality worldwide. Although vaccination programs and conventional antiviral therapies can reduce disease burden, increasing resistance to conventional therapies renders much of the population susceptible to infection. The present study focuses on an important host protein target, tumor susceptibility gene 101 (TSG101), which is functionally exploited (hijacked) by certain enveloped viruses to facilitate viral budding and release. We find that influenza viruses depend on TSG101 for progeny virion morphogenesis in infected host cells. Antibody-binding studies revealed that TSG101 is exposed at the surface of influenza-infected cells but remains intracellular in uninfected cells. Using recombinant TSG101 and influenza M1 protein, we demonstrated a direct interaction between these proteins involving the ubiquitin E2 variant domain of TSG101. These findings identify an interaction between TSG101 and M1 protein in infected cells. Furthermore, a monoclonal antibody directed against TSG101 reduced virus yields in cell-based assessment of influenza virus infection, underscoring the potential of the TSG101-M1 interaction as a possible antiviral therapeutic target. The display of TSG101 at the surface of infected cells, combined with evidence that TSG101 antibodies reduce virus yields, suggest that TSG101 plays an essential role in the budding process of influenza virus. Our findings may also suggest potential opportunities for influenza treatment and prevention by using monoclonal antibody therapeutics to interfere with virus replication.

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Section: Discussionsupporting

confidence: 73%

Antibody targeting of TSG101 on influenza-infected cells

Kinch¹

2010

VAAT

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“…Farklı yapısal özellikleri inceleyen çalışmalara göre coronovirüsler farklı büyüklüklerde (80-120 nm) ve şekillerde küreye benzer şekilde pleomorfik (farklı morfolojik biçimlerde) partiküller oluşturmaktadırlar (5,22,24,25).…”

Section: Coronavirüslerin Genel öZellikleriunclassified

“…Bütün zarflı proteinler ve N proteini virionların tamamında bulunmaktadır (23). Ayrıca, bu proteinlerin aralarındaki etkileşim sayesinde virüs partiküllerinin bir araya toplandığı düşünülmektedir (5,25).…”

Section: Coronavirüslerin Genel öZellikleriunclassified

Replication of coronavirus

2013

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ÖzetCoronavirüsler (CoVs) çok çeşitlilik gösteren bir virüs ailesidir. CoV'lar konak hücrelerle birçok aşamada etkileşime geçerler ve konak hücrenin değişik mekanizmalarını kullanarak enfeksiyonlarını ve replikasyonlarını gerçekleştirirler. CoV'ların moleküler biyolojisiyle ilgili olarak birçok şey bilinmektedir. Ancak CoV'ların moleküler biyolojisini daha iyi anlamak için daha çok bilgiye ihtiyaç vardır ve CoV'lara karşı geliştirilmiş herhangi etkili bir ilaç tedavisi bulunmamaktadır. CoV'ların moleküler biyolojisini daha iyi anlama adına son yıllarda yapılan araştırmalarda birçok teknik ve yöntem kullanılmıştır. Moleküler biyolojik araştırmalar açısından fare hepatit virüsü en çok çalışılan CoV'lardır ve Coronaviridae ailesi üyelerini araştırmak için iyi bir model sistemdir. Bu derleme CoV'lerin replikasyonunu, transkripsiyonunu ve tekrar bir araya getirilmesini anlatmaktadır. Anahtar kelimeler: Coronavirüs; replikasyon; transkripsiyon; toplanma Abstract Coronaviruses (CoVs) are a diverse family of viruses that interact at multiple levels with components of host cells taking this advantage of some of the cellular machineries for replication and proliferation. A lot is known about the molecular biology of CoVs but more information needs to be learned because no effective treatments against these viruses are available. The challenge now is to incorporate advance techniques in the investigative efforts done to understand further the biology of CoVs. In terms of molecular biology, mouse hepatitis virus (MHV) is the best-studied CoVs, and it is consequently considered a model system for the family of Coronaviridae. This review described replication, transcription, and assembly of CoVs.

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“…The genome also encodes three nonstructural proteins, which functions remain poorly understood. The assembly of coronavirus virions needs a concerted action of three structural proteins: the membrane protein (M), the small envelope protein (E), and the nucleocapsid protein (N) (de Haan & Rottier, 2005;Masters 2006). Among these three proteins, no role in pathogenesis has been reported for M and E.…”

Section: Murine Hepatitis Virus: An Agent Of Encephalitismentioning

confidence: 99%