Herpesvirus Flashcards
Structure of Herpes virus
- icosahderal enveloped with lipoprotien
- linear DsDNA
- has a tegument between the nucleocapsid and envelop containing regulatory protiens
-replicates in neculus - cause life long latent infections.
- only virus obtaing envelop from budding from nculear membrane
Symptoms groups of HerpesV
1- Vesicular rash for type1, type2 and VZV in primary infection and reactivation and primary infection is stronger
2- Multinucleated ginat cells in HSV1 and 2 and VZV and CV seen in lesions in Tznack smear
Catagories of herpesV based on cell infected and latency
1- Alpha: HSV1,2 and. VZV infect epithelial cells adn latent in neurons
2- Beta: CMV and HSV6 infect and latent in tissues
3-Gamma: EBV and HHV8 infect and latent in lymphoid cells
clinical findings by HSV1
1-Gingivostomatitis
2-Orolabial herpes or cold sores
3-Keratoconjuctivits
4-encephalitis
5-herpatic whitlow
6-Herpes gladiatorum
7-Eczema herpeticum with patients with atopci dermatitis
8-disseminated infections in immunocompormised patients with low T cell function.
all disease above the umblicius
9-erythema multiform
difference between HSV1 and HSV2
by restriction endonuclease patterns of their genoem DNA and type specific monoclonal antisera for glycoprotien G
- latency of HSV 1 is trigeminal ganglia
latency of HSV2 is in lumbar and sacral ganglia
Replication of HSV1 and HSV2
1- attach to heparn sulfate or nectin to enter
2-VP 16 tegument protien interacts with TF to make IE genes by RNA polymearse
3- IE whose mRNA is activated by protien brough by the incoming protien virion
4-E proties requrie synthesis of new viral regulatory protien to make their mRNA
5- making of HSV DNA is limited to few latecny associated transcripts (LATS) which suppress viral replication1- attach to heparan sulfate or nectin to enter
2- VP 16 tegument protein interacts with TF to make IE genes by RNA polymerase
3- IE whose mRNA is activated by protein brought by the incoming protein virion
4- E proteins require synthesis of new viral regulatory proteins to make their mRNA
5- making of HSV DNA is limited to few latency associated transcripts (LATS) which suppress viral replication
skin lesion progression of HSV1 and HSV2
Erythema-papule-vesicle-ulcer-crusts
clinical findings of HSV2
1- Genital herpes associated with fever and inguinal adenopathy
2-neonatla herpes from contact with vesicular lesions within brith
3-erythema multiform
Erythema multiform in HSV1 and HSV2
Centra red area surrounded by rign of normal skin making a bull eye lesions
- mostly macular or papular on trunk, hands and feet
eyrthema multiforme major
Stevens-Jhonson syndrome: fever, erosive oral lesions, extensive desquamating skin lesions by mycoplasma pneuoniae infection
Lab diagnosis of HSV1 and HSV2
PCR to distinguish between them
ELISA :Monoclonal antibody agaisnt Gycoprotien G
Tznack smear using Giemsa stain and seeing mutlinucleated giant cells
Treatment of HSV1 and HSV2
acyclovir for encephalitis and systemic disease by HSV1and neonatal infection by HSV2
nuceloside analogues like virptic for eye infection
oral acyclovir for HSV keratitis and recurrences of orolabial HSV1 infection
Prevention of HSV1 and HSV2
Valtrex and FAmvir to supress recurrent lesions
Varicella zostor virus charchterisics
-Varicella (chickenpox)Zoster(shingles)
- transmitted by respiratory droplets and direct contact with lesions
-one serotype
Patogensis and immunity of VZV
infects mucosa of upper RT and spreads via blood to skin making typical vesicular rahs
- multinucleated giant cells with intranuclear inclusions at base of lesions
- latency in dorsal root ganglia
Clincal findings of VZV
incubation period of 2 to 3 weeks
papulovesciular rash in crops on trunck and spread to head and extermities
- puritis
-Reyes syndrome: encephalopahty, liver degenration
-Postherpetic neurlagia (PNH)
Rash progression in VZV
papule-vesicle-pustule and crusts and finally scars
Treatment of VZV
Acyclovir or foscarnet
Prevention of VZV
Varivax–> varicella
Zostavax and shingrix for zoster
Virivax and zostavax are live atteunated
shingrix is recombinant vaccine
-VZIG for prophylaxis
CMV transmission
transmitted through placenta within the birth canal
- breastmilk
-saliva most common
-sexullay in semen and cervical secretions
- blood transfusion and organ transplants
CMV pathogenesis and immunity
- Multinucleated giant cells with prominent intranuclear inclusions
- reactivation in cervical cells
- assembly of MHC1 is unstable so no viral antigens are displayed
- encodes microRNA to prevent translation of mRNA for MHC1
CMV clincal findings IMP
- microcephaly, seiuzure, deafness, jaundice, purapura
- BLUEBERRY Muffin due to thrombocytopenia
-hepatosplenomegally
-heterophil negative mononucleosis - intracble coloits with diarrhea in AIDS patient
CMV treatment
- Ganciclovir for CMV retinitis and pneumonia
-valganciclovir
-foscarent
-cidofovir
-vitravene
EBV charchterstics
it causes infectious mononucleosis
- the most importatn antigen is viral capsid antigenE
- it enter B cells at site of receptor for C3 component
EBV antigens types
EA: made prior to viral DNA synthesis
EBNA: located in nucleus bound to chormosmome and diagnositic
Lymphocyte determined membrane antigen
viral membrane antigen
transmission of EBV
saliva, blood
Pathogenisis and immunity
- infection first in propharynx then to blood then to B cells
- IgM for VCA is the first response ( acute infection)
-IgG for VCA follows and persists for life ( prior infection)
Clinical findings of EBV
infectous mononucleaosis with fever, sore thoratm, lymphadenopathy and splenomegaly, anorexia and latheragy. hairy leukoplakia and hepatosplenomegaly
- hepatitis and encephalitis
- splenic rupture assocaited with contact support
- assoacited with X linked lymphoproliferative syndrome
- assoaicted with burkitss, hodkins and nasopharyneal carcinoma
lab diagnosis of EBV
1- heterophil antibody test for early diagnosis
2- EBV specific antibody test for difficult cases
HHV8 kaposi sacroma
common cancer in AIDS patients who acquired AIDS seaully
resembles lymphotropic herpes like HSV and VZV
clinical findings of HHV8
causes malignant transformation by inactivation of tumor supressor gene by LANA inactivating RB and P53
