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Virus

About: Virus is a research topic. Over the lifetime, 136914 publications have been published within this topic receiving 5209107 citations. The topic is also known as: infectious agent & viruses.


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Journal ArticleDOI
TL;DR: This work has shown that viral genetic diversity is determined by multiple virus- and host-dependent processes, and that viral mutation rates can evolve in response to specific selective pressures.
Abstract: The remarkable capacity of some viruses to adapt to new hosts and environments is highly dependent on their ability to generate de novo diversity in a short period of time. Rates of spontaneous mutation vary amply among viruses. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post-replicative repair. Additionally, massive numbers of mutations can be introduced by some virus-encoded diversity-generating elements, as well as by host-encoded cytidine/adenine deaminases. Our current knowledge of viral mutation rates indicates that viral genetic diversity is determined by multiple virus- and host-dependent processes, and that viral mutation rates can evolve in response to specific selective pressures.

585 citations

Journal ArticleDOI
TL;DR: The emerging understanding of virus population dynamics, the role of the immune system in limiting virus abundance, the dynamics of viral drug resistance, and the question of whether virus infection can be eliminated from individual patients by drug treatment are discussed.
Abstract: The recent development of potent antiviral drugs not only has raised hopes for effective treatment of infections with HIV or the hepatitis B virus, but also has led to important quantitative insights into viral dynamics in vivo. Interpretation of the experimental data depends upon mathematical models that describe the nonlinear interaction between virus and host cell populations. Here we discuss the emerging understanding of virus population dynamics, the role of the immune system in limiting virus abundance, the dynamics of viral drug resistance, and the question of whether virus infection can be eliminated from individual patients by drug treatment.

584 citations

Journal ArticleDOI
18 May 2010-Mbio
TL;DR: The construction of a novel immunogen comprising the conserved influenza HA stalk domain and lacking the globular head is described, which shows that vaccination of mice with a headless HA confers protection to these animals against a lethal influenza virus challenge, and predicts that a single immunization with aHeadless HA vaccine will offer effective protection through several influenza epidemics.
Abstract: Although highly effective in the general population when well matched to circulating influenza virus strains, current influenza vaccines are limited in their utility due to the narrow breadth of protection they provide. The strain specificity of vaccines presently in use mirrors the exquisite specificity of the neutralizing antibodies that they induce, that is, antibodies which bind to the highly variable globular head domain of hemagglutinin (HA). Herein, we describe the construction of a novel immunogen comprising the conserved influenza HA stalk domain and lacking the globular head. Vaccination of mice with this headless HA construct elicited immune sera with broader reactivity than those obtained from mice immunized with a full-length HA. Furthermore, the headless HA vaccine provided full protection against death and partial protection against disease following lethal viral challenge. Our results suggest that the response induced by headless HA vaccines is sufficiently potent to warrant their further development toward a universal influenza virus vaccine.

584 citations

BookDOI
01 Jan 1989
TL;DR: Among the most significant accomplish ments in influenza virus research has been the delineation of the three dimensional structure of the two surface glycoproteins of the virus, the hemagglutinin and neuraminidase, which provided a structural basis for mapping both the antigenic sites and the regions involved in the major biological functions of these two molecules.
Abstract: Influenza virus is an important human pathogen, frequently causing widespread disease and a significant loss of life. Much has been learned about the structure of the virus, its genetic variation, its mode of gene expression and replication, and its interaction with the host immu nologic system. This knowledge has the potential of leading to ap proaches for the control of influenza virus. In addition, research on influ enza virus has led to important advances in eukaryotic molecular and cellular biology and in immunology. A major focus of this book is the molecular biology of influenza virus. The first chapter, which serves as an introduction, describes the structure of each of the genomic RNA segments and their encoded pro teins. The second chapter discusses the molecular mechanisms involved in the expression and replication of the viral genome. In addition to other subjects, this chapter deals with one of the most distinctive features of influenza virus, namely the unique mechanism whereby viral messenger RNA synthesis is initiated by primers deaved from newly synthesized host-cell RNAs in the nudeus. Among the most significant accomplish ments in influenza virus research has been the delineation of the three dimensional structure of the two surface glycoproteins of the virus, the hemagglutinin and neuraminidase. This has provided a structural basis for mapping both the antigenic sites and the regions involved in the major biological functions of these two molecules."

582 citations

Journal ArticleDOI
TL;DR: It is proposed that the interaction of E6 with IRF-3 and the inhibition of IRf-3's transcriptional activity may provide the virus a means to circumvent the normal antiviral response of an HPV16-infected cell.
Abstract: Interferon regulatory factor-3 (IRF-3) was found to specifically interact with HPV16 E6 in a yeast two-hybrid screen. IRF-3 is activated by the presence of double-stranded RNA or by virus infection to form a stable complex with other transcriptional regulators that bind to the regulatory elements of the IFNβ promoter. We show that IRF-3 is a potent transcriptional activator and demonstrate that HPV16 E6 can inhibit its transactivation function. The expression of HPV16 E6 in primary human keratinocytes inhibits the induction of IFNβ mRNA following Sendai virus infection. The binding of HPV16 E6 to IRF-3 does not result in its ubiquitination or degradation. We propose that the interaction of E6 with IRF-3 and the inhibition of IRF-3’s transcriptional activity may provide the virus a means to circumvent the normal antiviral response of an HPV16-infected cell.

582 citations


Network Information
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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20242
20234,275
20228,706
20213,455
20203,848
20193,309