Herpes viruses
Immunity to Herpes Simplex Virus
Category: Virology | Immunology
from Keith R. Jerome writing in Alphaherpesviruses: Molecular Virology:
HSV presents unique challenges to the human immune system. Most of these result from the ability of the virus to establish latency in neurons of the dorsal root ganglia. The first line of defense against the initial establishment of latent infection is the innate immune response. The innate response relies on a variety of cell types recognizing HSV infection via pattern recognition receptors, including toll-like receptors. After exposure, the adaptive immune response is triggered. However, the adaptive response must deal with reactivation of HSV from the latently infected neuron, which in turn seeds mucosal sites with virus. T cells are especially important in this, and likely control both the extent of reactivation from latently infected neurons as well as the extent of viral replication at mucosal sites. Not surprising, HSV has evolved a wide variety of immune evasion mechanisms to tip this balance in its favor and facilitate transmission to new hosts. The study of HSV and its interaction with the host immune system has provided insights into the function of both, and may ultimately facilitate the development of an effective HSV vaccine.
Further reading: Alphaherpesviruses: Molecular Virology
HSV presents unique challenges to the human immune system. Most of these result from the ability of the virus to establish latency in neurons of the dorsal root ganglia. The first line of defense against the initial establishment of latent infection is the innate immune response. The innate response relies on a variety of cell types recognizing HSV infection via pattern recognition receptors, including toll-like receptors. After exposure, the adaptive immune response is triggered. However, the adaptive response must deal with reactivation of HSV from the latently infected neuron, which in turn seeds mucosal sites with virus. T cells are especially important in this, and likely control both the extent of reactivation from latently infected neurons as well as the extent of viral replication at mucosal sites. Not surprising, HSV has evolved a wide variety of immune evasion mechanisms to tip this balance in its favor and facilitate transmission to new hosts. The study of HSV and its interaction with the host immune system has provided insights into the function of both, and may ultimately facilitate the development of an effective HSV vaccine.
Further reading: Alphaherpesviruses: Molecular Virology
Strategies Against Herpes Simplex Virus
from Timothy E. Dudek and David M. Knipe writing in Alphaherpesviruses: Molecular Virology:
Vaccines have been among the most effective public health approaches for protecting individuals against viral disease, with two of the world's most successful vaccines being against smallpox virus and poliovirus. Herpes simplex virus 1 (HSV-1) is a nearly ubiquitous pathogen, and the worldwide prevalence of herpes simplex virus 2 (HSV-2) continues to increase. These two pathogens cause significant morbidity and mortality among the general population, but in particular in neonates and immunocompromised individuals. Perhaps most significantly, there is a 3-4 fold increased risk of HIV acquisition in HSV-2 infected individuals. To date, attempts at producing a vaccine against HSV have not been successful, but each attempt has brought insights into what may be required for an effective vaccine. Furthermore, intense studies into the immunology of HSV infection and the resources that have been put into vaccine design and development have recently yielded knowledge that will be necessary to achieve the goal of a highly effective vaccine against HSV.
Further reading: Alphaherpesviruses: Molecular Virology
Vaccines have been among the most effective public health approaches for protecting individuals against viral disease, with two of the world's most successful vaccines being against smallpox virus and poliovirus. Herpes simplex virus 1 (HSV-1) is a nearly ubiquitous pathogen, and the worldwide prevalence of herpes simplex virus 2 (HSV-2) continues to increase. These two pathogens cause significant morbidity and mortality among the general population, but in particular in neonates and immunocompromised individuals. Perhaps most significantly, there is a 3-4 fold increased risk of HIV acquisition in HSV-2 infected individuals. To date, attempts at producing a vaccine against HSV have not been successful, but each attempt has brought insights into what may be required for an effective vaccine. Furthermore, intense studies into the immunology of HSV infection and the resources that have been put into vaccine design and development have recently yielded knowledge that will be necessary to achieve the goal of a highly effective vaccine against HSV.
Further reading: Alphaherpesviruses: Molecular Virology
Nucleocapsid of Herpes Simplex Virus
Category: Virology
from James F. Conway and Fred L. Homa writing in Alphaherpesviruses: Molecular Virology:
The herpes simplex virion consists of an external membrane envelope, a proteinaceous layer called the tegument, and an icosahedral capsid containing the double-stranded linear DNA genome. The capsid shell is 125 nm in diameter and consists of 162 capsomers (150 hexons, 11 pentons and a portal) which lie on a T=16 icosahedral lattice. The capsid shell consists of four major structural proteins VP5, VP19C, VP23 and VP26 which are the products of the HSV UL19, UL38, UL18 and UL35 genes. In addition to the four major structural proteins the HSV-1 capsid contains a number of minor capsid proteins. These include the UL6, UL15, UL17, UL25, UL28 and UL33 proteins, all of which (along with the HSV-1 UL32 protein) are required for the processing and packaging of replicated viral DNA into preformed capsid shells. The UL6, UL17, UL25 and UL33 proteins remain associated with DNA containing capsids while UL15 and UL28 do not. A recent review summarizes the present knowledge with respect to how the capsid is assembled, how DNA is packaged and what is known about the role of the seven packaging proteins in this process. In addition, recent advances in our understanding the structure of the four distinct types of capsids that are present in HSV infected cells as determined by three dimensional image reconstructions from cryo¬-electron microscopy (cryoEM) are presented and discussed.
Further reading: Alphaherpesviruses: Molecular Virology
The herpes simplex virion consists of an external membrane envelope, a proteinaceous layer called the tegument, and an icosahedral capsid containing the double-stranded linear DNA genome. The capsid shell is 125 nm in diameter and consists of 162 capsomers (150 hexons, 11 pentons and a portal) which lie on a T=16 icosahedral lattice. The capsid shell consists of four major structural proteins VP5, VP19C, VP23 and VP26 which are the products of the HSV UL19, UL38, UL18 and UL35 genes. In addition to the four major structural proteins the HSV-1 capsid contains a number of minor capsid proteins. These include the UL6, UL15, UL17, UL25, UL28 and UL33 proteins, all of which (along with the HSV-1 UL32 protein) are required for the processing and packaging of replicated viral DNA into preformed capsid shells. The UL6, UL17, UL25 and UL33 proteins remain associated with DNA containing capsids while UL15 and UL28 do not. A recent review summarizes the present knowledge with respect to how the capsid is assembled, how DNA is packaged and what is known about the role of the seven packaging proteins in this process. In addition, recent advances in our understanding the structure of the four distinct types of capsids that are present in HSV infected cells as determined by three dimensional image reconstructions from cryo¬-electron microscopy (cryoEM) are presented and discussed.
Further reading: Alphaherpesviruses: Molecular Virology
Herpes Simplex Virus Regulatory Protein ICP4
Category: Virology | Regulation
ICP4 is expressed from the HSV genome very early in infection. It is a large structurally complex nuclear phosphoprotein that is essential for viral growth largely due to its requirement for the transcriptional activation of most HSV early and late genes. It also acts a repressor of transcription under certain circumstances. The HSV genome is transcribed by RNA polII, and ICP4 interacts with components of the RNA polII transcription machinery to carry out is functions in transcription. The interactions that are important for its functions can be genetically defined implicating a modular composition of the ICP4 protein. ICP4 also plays a specific role in virus growth in sympathetic neurons implicating a specific function in pathogenesis. A recent review describes what is known about ICP4 from many genetic, biological and biochemical studies, from many laboratories.
Further reading: Alphaherpesviruses: Molecular Virology
Further reading: Alphaherpesviruses: Molecular Virology
EBV
A new publication on EBV: Epstein-Barr Virus: Latency and Transformation was published recently. In this book, expert EBV virologists comprehensively review this important subject from a genetic, biochemical, immunological, and cell biological perspective. Topics include: latent infections, EBV leader protein, EBNA-1 in viral DNA replication and persistence, EBNA-2 in transcription activation of viral and cellular genes, the nuclear antigen family 3 in regulation of cellular processes, molecular profiles of EBV latently infected cells, latent membrane protein 1 oncoprotein, regulation of latency by LMP2A, role of noncoding RNAs in EBV-induced cell growth and transformation and the regulation of EBV latency by viral lytic proteins. This book is essential reading for all EBV virologists as well as clinical and basic scientists working on oncogenic viruses read more ...
 | Edited by: Erle S. Robertson ISBN: 978-1-904455-62-2 Publisher: Caister Academic Press Publication Date: April 2010 Cover: Hardback read more ... |