Herpesviridae

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Herpesviridae
Virus classification Edit this classification
(unranked): Virus
Realm: Duplodnaviria
Kingdom:
Heunggongvirae
Phylum: Peploviricota
Class: Herviviricetes
Order: Herpesvirales
Family: Orthoherpesviridae
Subfamilies and genera

See text

Herpesviridae is a large

International Committee on the Taxonomy of Viruses (ICTV) established Herpesvirus as a genus with 23 viruses among four groups.[5] As of 2020, 115 species are recognized, all but one of which are in one of the three subfamilies.[6] Herpesviruses can cause both latent and lytic
infections.

Nine herpesvirus types are known to primarily infect humans,

human herpesvirus 7 (HHV-7), and Kaposi's sarcoma-associated herpesvirus (KSHV, also known as HHV-8).[7]
HHV here stands for "Human Herpesvirus".

In total, more than 130 herpesviruses are known,

pustular vulvovaginitis
.

Taxonomy

Additionally, the species Iguanid herpesvirus 2 is currently unassigned to a genus and subfamily.[6]

See Herpesvirales#Taxonomy for information on taxonomic history, phylogenetic research, and the nomenclatural system.

Structure

Schematic drawing of a Herpesviridae virion

All members of the Herpesviridae share a common structure; a relatively large, monopartite, double-stranded, linear

virion
. The structural components of a typical HSV virion are the Lipid bilayer envelope, Tegument, DNA, Glycoprotein spikes and Nucleocapsid. The four-component Herpes simplex virion encompasses the double-stranded DNA genome into an icosahedral nucleocapsid. There is tegument around. Tegument contains filaments, each 7 nm wide. It is an amorphous layer with some structured regions. Finally, it is covered with a lipoprotein envelope. There are spikes made of glycoprotein protruding from each virion. These can expand the diameter of the virus to 225 nm. The diameters of virions without spikes are around 186 nm. There are at least two unglycosylated membrane proteins in the outer envelope of the virion. There are also 11 glycoproteins. These are gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL and gM. Tegument contains 26 proteins. They have duties such as capsid transport to the nucleus and other organelles, activation of early gene transcription, and mRNA degradation. The icosahedral nucleocapsid is similar to that of tailed bacteriophage in the order Caudovirales. This capsid has 161 capsomers consisting of 150 hexons and 11 pentons, as well as a portal complex that allows entry and exit of DNA into the capsid.[12][13]

Life cycle

All herpesviruses are nuclear-replicating—the viral

nucleus.[citation needed
]

Infection is initiated when a viral particle contacts a cell with specific types of

transcription of viral genes occurs.[citation needed
]

During symptomatic infection, infected cells transcribe

latency-associated transcript (LAT) accumulate, instead. In this fashion, the virus can persist in the cell (and thus the host) indefinitely. While primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free.[citation needed
]

Chromatin dynamics regulate the transcription competency of entire herpes virus genomes. When the virus enters a cell, the cellular immune response is to protect the cell. The cell does so by wrapping the viral DNA around histones and condensing it into chromatin, causing the virus to become dormant, or latent. If cells are unsuccessful and the chromatin is loosely bundled, the viral DNA is still accessible. The viral particles can turn on their genes and replicate using cellular machinery to reactivate, starting a lytic infection.[14]

Reactivation of latent viruses has been implicated in a number of diseases (e.g.

nonspecific symptoms, such as low-grade fever, headache, sore throat, malaise, and rash, as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells.[citation needed
]

In animal models, local trauma and system stress have been found to induce reactivation of latent herpesvirus infection. Cellular stressors like transient interruption of protein synthesis and hypoxia are also sufficient to induce viral reactivation.[15]

Genus Subfamily Host details Tissue tropism Entry details Release details Replication site Assembly site Transmission
Iltovirus α Birds: galliform: psittacine None Cell receptor endocytosis Budding Nucleus Nucleus Oral-fecal, aerosol
Proboscivirus β Elephants None Glycoproteins Budding Nucleus Nucleus Contact
Cytomegalovirus β Humans; monkeys Epithelial mucosa, hematopoietic (blood) lineage cells Glycoproteins Budding Nucleus Nucleus Urine, saliva
Mardivirus α Chickens; turkeys; quail None Cell receptor endocytosis Budding Nucleus Nucleus Aerosol
Rhadinovirus γ Humans; mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Sex, saliva
Macavirus γ Mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Sex, saliva
Roseolovirus β Humans T-cells; B-cells; NK-cell; monocytes; macrophages; epithelial Glycoproteins Budding Nucleus Nucleus Respiratory contact
Simplexvirus α Humans; mammals Epithelial mucosa Cell receptor endocytosis Budding Nucleus Nucleus Sex, saliva
Scutavirus α Sea turtles None Cell receptor endocytosis Budding Nucleus Nucleus Aerosol
Varicellovirus α Mammals Epithelial mucosa Glycoproteins Budding Nucleus Nucleus Aerosol
Percavirus γ Mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Sex, saliva
Lymphocryptovirus γ Humans; mammals B-lymphocytes Glycoproteins Budding Nucleus Nucleus Saliva
Muromegalovirus β Rodents Salivary glands Glycoproteins Budding Nucleus Nucleus Contact

Evolution

The three mammalian subfamilies – Alpha-, Beta- and Gamma-herpesviridae – arose approximately 180 to 220 mya.[16] The major sublineages within these subfamilies were probably generated before the mammalian radiation of 80 to 60 mya. Speciations within sublineages took place in the last 80 million years probably with a major component of cospeciation with host lineages.[citation needed]

All the currently known bird and reptile species are alphaherpesviruses. Although the branching order of the herpes viruses has not yet been resolved, because herpes viruses and their hosts tend to coevolve this is suggestive that the alphaherpesviruses may have been the earliest branch.[citation needed]

The time of origin of the genus Iltovirus has been estimated to be 200 mya while those of the mardivirus and simplex genera have been estimated to be between 150 and 100 mya.[17]

Immune system evasions

Herpesviruses are known for their ability to establish lifelong infections. One way this is possible is through immune evasion. Herpesviruses have many different ways of evading the immune system. One such way is by encoding a protein mimicking human interleukin 10 (hIL-10) and another is by downregulation of the major histocompatibility complex II (MHC II) in infected cells.

cmvIL-10

Research conducted on cytomegalovirus (CMV) indicates that the viral human IL-10 homolog, cmvIL-10, is important in inhibiting

PBMC) to both increase and decrease in proliferation whereas cmvIL-10 only causes a decrease in proliferation of PBMCs. This indicates that cmvIL-10 may lack the stimulatory effects that hIL-10 has on these cells.[18]

It was found that cmvIL-10 functions through phosphorylation of the

PKB (Akt). PKB may then activate mTOR, which may target Stat3 for phosphorylation on the S727 residue.[19]

MHC downregulation

Another one of the many ways in which herpes viruses evade the immune system is by down regulation of

MHC II. This is observed in almost every human herpesvirus. Down regulation of MHC I and MHC II can come about by many different mechanisms, most causing the MHC to be absent from the cell surface. As discussed above, one way is by a viral chemokine homolog such as IL-10. Another mechanism to down regulate MHCs is to encode viral proteins that detain the newly formed MHC in the endoplasmic reticulum (ER). The MHC cannot reach the cell surface and therefore cannot activate the T cell response. The MHCs can also be targeted for destruction in the proteasome or lysosome. The ER protein TAP also plays a role in MHC down regulation. Viral proteins inhibit TAP preventing the MHC from picking up a viral antigen peptide. This prevents proper folding of the MHC and therefore the MHC does not reach the cell surface.[20]

Human herpesvirus types

Below are the nine distinct viruses in this family known to cause disease in humans.[21][22][23]

Human herpesvirus (HHV) classification[1][22]
Name Synonym Subfamily Primary Target Cell Syndrome Site of Latency Means of Spread
HHV‑1 Herpes simplex virus-1 (HSV-1) α (Alpha) Mucoepithelial
herpes simplex
infections		 Neuron (sensory ganglia) Close contact (oral or sexually transmitted infection)
HHV-2 Herpes simplex virus-2 (HSV-2) α Mucoepithelial Oral and/or genital herpes, herpetic gingivostomatitis, pharyngitis, eczema herpeticum, herpetic whitlow, herpes simplex keratitis, erythema multiforme, Mollaret's meningitis, as well as other herpes simplex infections Neuron (sensory ganglia) Close contact (oral or sexually transmitted infection)
HHV-3 Varicella zoster virus (VZV) α Mucoepithelial
shingles
 Neuron (sensory ganglia) Respiratory and close contact (including sexually transmitted infection)
HHV-4 Epstein–Barr virus (EBV) Lymphocryptovirus γ (Gamma)
epithelial cells
Epstein–Barr virus-associated aggressive NK cell leukemia, CNS lymphoma in AIDS patients, post-transplant lymphoproliferative syndrome (PTLD), nasopharyngeal carcinoma, HIV-associated hairy leukoplakia, multiple sclerosis
 B cell Close contact, transfusions, tissue transplant, and congenital
HHV-5 Cytomegalovirus (CMV) β (Beta)
epithelial cells
 Infectious mononucleosis-like syndrome,[24] retinitis Monocyte, and ? Saliva, urine, blood, breast milk
HHV-6A and 6B Roseolovirus β T cells and ? Sixth disease (
roseola infantum
or exanthem subitum)		 T cells and ? Respiratory and close contact?
HHV-7
 β T cells and ? drug-induced hypersensitivity syndrome, encephalopathy, hemiconvulsion-hemiplegia-epilepsy syndrome, hepatitis infection, postinfectious myeloradiculoneuropathy, pityriasis rosea, and the reactivation of HHV-4 (EBV), leading to "mononucleosis-like illness" T cells and ? ?
HHV-8 Kaposi's sarcoma-associated herpesvirus
(KSHV), a type of Rhadinovirus		 γ Lymphocyte and other cells
Castleman's disease
 B cell Close contact (sexual), saliva?

Zoonotic herpesviruses

In addition to the herpesviruses considered endemic in humans, some viruses associated primarily with animals may infect humans. These are zoonotic infections:

Zoonotic herpesviruses
Species Type Synonym Subfamily Human Pathophysiology
Macaque monkey
 CeHV-1 Cercopithecine herpesvirus 1, (
monkey B virus
)		 α Very unusual, with only approximately 25 human cases reported.[25] Untreated infection is often deadly; sixteen of the 25 cases resulted in fatal encephalomyelitis. At least four cases resulted in survival with severe neurologic impairment.[25][26] Symptom awareness and early treatment are important for laboratory workers facing exposure.[27]
Mouse MuHV-4
Murid herpesvirus 68
 (MHV-68)		 γ
false positive results, due to antibody cross-reaction with other herpesviruses.[28]

Animal herpesviruses

In

avian infectious laryngotracheitis virus is phylogenetically distant from these two viruses and serves to underline similarity and diversity within the Alphaherpesvirinae.[2][3]

Research

Main article: Herpes simplex research

Research is currently ongoing into a variety of side-effect or co-conditions related to the herpesviruses. These include:

See also

References

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  12. ^ Liu, Y., Jih, J., Dai, X. et al. Cryo-EM structures of herpes simplex virus type 1 portal vertex and packaged genome. Nature 570, 257–261 (2019). https://doi.org/10.1038/s41586-019-1248-6
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External links

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