Herpes - infections

Сентябрь 3, 2022

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Herpes - infections

Содержание

2. CLASSIFICATION Family : Herpesviridae Genus : Simplexvirus Subfamily : Alphaherpesvirinae Species : a) Herpes Simplex Virus
3. MORPHOLOGY Large , enveloped viruses containing double stranded DNA Virion : 120-300nm in diameter Icosadeltahedral protein
4. RESISTANCE Sensitive to: Acid Solvents Detergents Drying
5. ANTIGENIC STRUCTURE HSV 1 & HSV 2 differentiated by serologi typing and by DNA homology Distinguished
6. TRANSMISSION Generally transmitted by direct contact of lips or genitals when the sores are present, or
7. CELLULAR ENTRY Entry of HSV into the host cell involves interactions of several viral glycoproteins with
8. Replication In the case of Herpes virus, initial interactions occur when glycoprotein C, on the surface
9. REPLICATION After the viral envelope contents of capsid with tegument proteins has entered the cell via
10. REPLICATION
11. LATENT INFECTION Especially in neurons, Herpes may persist in a quiescent but persistent form known as
12. ENCAPSIDATION AND EGRESS The procapsid proteins (UL18, UL19 and UL38) assemble around scaffolding proteins (UL26 and
13. ENVELOPMENT & RELEASE Viral glycoproteins are translated from HSV RNA on the rough endoplasmic reticulum then
14. LABORATORY DIAGNOSIS Microscopical Scrapings of lesion: examined microscopically for multinucleated giant cell whose nuclei contain eosinophilic
15. Laboratory diagnosis Virological Rapid,definitive determination HSV is made by demonstrating in tissue : a) viral antigen
16. Laboratory diagnosis Serological Only useful for diagnosing primary HSV infection & epidemiological studies Not useful for
17. TREATMENT Anti HSC drugs like acyclovir, vidarabine, idoxuridine and trifluridine Act as inhibitors of viral DNA
20. Vesiculobullous eruption Herpetic Whitlow (HSV 1)
21. HSV in situ hybridization
23. Скачать презентацию

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CLASSIFICATION
Family : Herpesviridae
Genus : Simplexvirus
Subfamily : Alphaherpesvirinae
Species : a) Herpes Simplex

Virus 1 (HSV 1)
b) Herpes Simplex Virus 2 ( HSV 2)

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MORPHOLOGY
Large , enveloped viruses containing double stranded DNA
Virion : 120-300nm in

diameter
Icosadeltahedral protein capsid (average 100nm) consisting of 162 capsomeres, with core containg DNA genome
Amorphous proteinaceous layer : the tegument
Animation

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RESISTANCE
Sensitive to:
Acid
Solvents
Detergents
Drying

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ANTIGENIC STRUCTURE
HSV 1 & HSV 2 differentiated by serologi typing and

by DNA homology
Distinguished by cultivation on chick embro, by neuro virulence, clinical manisfestation, susceptibility to antiviral agents

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TRANSMISSION
Generally transmitted by direct contact of lips or genitals when the

sores are present, or also when no sores are present (known as viral shedding)
Present in semen, vaginal fluids, and saliva
Herpes may be transmitted during childbirth, which can be fatal to the infant.
Transmission occurs while passing through the birth canal and the risk of infection is minimal if there are no symptoms or exposed blisters during delivery.

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CELLULAR ENTRY
Entry of HSV into the host cell involves interactions of

several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell.
The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.

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Replication
In the case of Herpes virus, initial interactions occur when glycoprotein

C, on the surface of the viral envelope, binds to a cell surface particle, heparan sulfate. Glycoprotein D binds specifically to the herpesvirus entry mediator receptor (HVEM), thus providing a strong, fixed attachment to the host cell. These interactions bring the membrane surfaces into mutual proximity and allow for other surface glycoproteins to interact.
Once bound to the HVEM, glycoprotein D changes its conformation and interacts with glycoproteins H and L, which form a complex. The interaction of these membrane proteins results in the hemifusion state. Afterward, glycoprotein B interaction with the glycoprotein H and L complex creates an entry pore.Glycoprotein B interacts with host cell surface glycosaminoglycans.
Animation

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REPLICATION
After the viral envelope contents of capsid with tegument proteins has

entered the cell via the entry pore, the viral particles migrate to the nucleus, where the genome is replicated using enzymes from the host cell. Upon entering the cell, an α-TIF protein also joins the viral particle and aids in immediate early transcription.The virion host shutoff protein (VHF-UL41) is very important to viral replication. This enzyme shuts off protein synthesis in the host, degrades host mRNA, helps in viral replication, and regulates gene expression of viral proteins. While the viral genome immediately travels to the nucleus, the VHF protein remains in the cytoplasm.
The packaging of the viral particles, which include the genome, core and the capsid, occur in the nucleus. In the nucleus, cleavage of genome concatemers occurs and these are placed into pre-formed capsids. The viral envelope is acquired from the nuclear envelope, more specifically the inner lamellae of the membrane
Animation

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REPLICATION

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LATENT INFECTION
Especially in neurons, Herpes may persist in a quiescent but

persistent form known as latent infection.
During latent infection of a cell, Herpes virus express Latency Associated Transcript (LAT) RNA.
LAT is known to regulate the host cell genome and interferes with natural cell death mechanisms.
By maintaining the host cells, LAT preserves a reservoir for the virus, which allows later recurrences to produce further infections.
Animation

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ENCAPSIDATION AND EGRESS
The procapsid proteins (UL18, UL19 and UL38) assemble around

scaffolding proteins (UL26 and UL26.5) that are then digested away.
The empty capsid incorporates DNA by means of the action of cleavage/packaging proteins
The capsid migrates to the nuclear membrane and buds into the lumen between the inner and outer nuclear membrane.
This enveloped virion then enters the cytoplasm through fusion with the outer nuclear membrane.
Animation

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ENVELOPMENT & RELEASE
Viral glycoproteins are translated from HSV RNA on the

rough endoplasmic reticulum then transported to the golgi body in vesicles to continue the glycosylation process. The glycoproteins are then transported in vesicles to the nuclear or plasma membrane.
The HSV capsid associates with tegument proteins then acquires a mature envelope by budding into an exocytotic vesicle. The enveloped infectious virion migrates to the virus modified membrane and is released outside of the cell.
Animation

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LABORATORY DIAGNOSIS
Microscopical
Scrapings of lesion: examined microscopically for multinucleated giant cell whose

nuclei contain eosinophilic inclusions (Cowdry type A inclusions)

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Laboratory diagnosis
Virological
Rapid,definitive determination HSV is made by demonstrating in tissue :
a)

viral antigen : - immunofluorescence
- immunoperoxidase method
b) DNA : - in situ hybridization

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Laboratory diagnosis
Serological
Only useful for diagnosing primary HSV infection & epidemiological studies
Not

useful for diagnosing recurrent disease due to a significant rise in Ab titers are not usually accompany recurrent disease

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TREATMENT
Anti HSC drugs like acyclovir, vidarabine, idoxuridine and trifluridine
Act as

inhibitors of viral DNA synthesis

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Vesiculobullous eruption
Herpetic Whitlow (HSV 1)

Слайд 21

Herpes - infections

Содержание

CLASSIFICATIONFamily : HerpesviridaeGenus : SimplexvirusSubfamily : AlphaherpesvirinaeSpecies : a) Herpes Simplex

MORPHOLOGYLarge , enveloped viruses containing double stranded DNAVirion : 120-300nm in

RESISTANCESensitive to:AcidSolventsDetergents Drying

ANTIGENIC STRUCTUREHSV 1 & HSV 2 differentiated by serologi typing and

TRANSMISSIONGenerally transmitted by direct contact of lips or genitals when the

CELLULAR ENTRYEntry of HSV into the host cell involves interactions of

ReplicationIn the case of Herpes virus, initial interactions occur when glycoprotein

REPLICATIONAfter the viral envelope contents of capsid with tegument proteins has

REPLICATION

LATENT INFECTIONEspecially in neurons, Herpes may persist in a quiescent but

ENCAPSIDATION AND EGRESSThe procapsid proteins (UL18, UL19 and UL38) assemble around

ENVELOPMENT & RELEASEViral glycoproteins are translated from HSV RNA on the

LABORATORY DIAGNOSISMicroscopicalScrapings of lesion: examined microscopically for multinucleated giant cell whose

Laboratory diagnosisVirologicalRapid,definitive determination HSV is made by demonstrating in tissue : a)

Laboratory diagnosisSerologicalOnly useful for diagnosing primary HSV infection & epidemiological studiesNot

TREATMENT Anti HSC drugs like acyclovir, vidarabine, idoxuridine and trifluridineAct as

Vesiculobullous eruptionHerpetic Whitlow (HSV 1)

HSV in situ hybridization

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