Herpes Virus

Question 1

Herpesviruses

Structure

Answer 1

enveloped, icosahedral, dsDNA

Question 2

Herpesvirus Transcription`

Answer 2

Transcription – temporal, uses host RNA polymerase II

Question 3

Herpesvirus α proteins

Answer 3

α proteins – immediate early, involved in transcription regulation

Question 4

Herpesvirus β proteins

Answer 4

β proteins – early, for DNA replication, DNA polymerase

Question 5

Herpesvirus γ proteins

Answer 5

γ proteins – late, structural components

Question 6

Herpesvirus Envelope

Answer 6

Envelope – buds through exocytic vesicle to obtain double envelope

Question 7

Herpesvirus Alpha: HHV-1 – HSV1

Answer 7

infect mucoepithelial cells of mouth/genitals → saliva transmission, autoinoculation
Epidemiology – early childhood, 90% seropositive by age of 10
Latency – CN5, superior cervical, and CN10 ganglia

Question 8

Herpes virus Alpha: HHV-2 – HSV2,

Answer 8

infect mucoepithelial cells of mouth/genitals → sexual contact, autoinoculation
Latency – sacral ganglia

Question 9

Labialis

Answer 9

Labialis – cold sores due to stress, UV light, trauma, menstruation

Question 10

Whitlow

Answer 10

Whitlow – infection of hands and wrists due to transfer of virus into cuts/sores

Question 11

Genital herpes

Answer 11

Genital herpes – mostly HSV2, shaft or glans of penis, vulva, vagina, cervix, inner thighs

Question 12

Eczema herpeticum

Answer 12

Eczema herpeticum – children with atopic dermatitis, burn pts → cutaneous viral spread and to liver and adrenal glands

Question 13

Herpes gladiatorum

Answer 13

Herpes gladiatorum – mostly due to HSV1, superficial skin lesions, common in wrestlers

Question 14

Keratoconjunctivitis

Answer 14

Keratoconjunctivitis – HSV1, unilateral inflammation, recurrent activation can lead to cornea damage and blindness

Question 15

Encephalitis

Answer 15

– lesions of temporal and inferior frontal lobes, → neutros early → macros and lymphos later, hemorrhage from viral replication → fever, confusion, coma, seizures, Cowdry A inclusions

Question 16

Neonatal herpes

Answer 16

– almost always HSV2, usually fatal, acquired in utero or during birth → spread to lungs, liver, CNS

Question 17

HHV-3

Answer 17

HHV-3 – varicella zoster → chicken pox (2-6 yr peak) and herpes zoster (shingles) Latency – sensory ganglia

Question 18

HHV-3 Transmission

Answer 18

Transmission – droplets → lungs → lymphatics → liver, spleen, macros → mucous membranes (contagious), viremia → skin, latency

Question 19

HHV-3 Congenital Varicella

Answer 19

Congenital varicella – mother is infected during first trimester → scarring of skin, limb hypoplasia, CNS/eye defects, 35% mortality

Question 20

HHV-3 Treatment

Answer 20

Treatment – acyclovir, valacyclovir (↑ bioaval), penciclovir/famciclovir (eye, skin), trifluorothymidine (eye), live VSV vaccine (OKA, Zostavax)

Question 21

HHV-3 Diagnosis

Answer 21

Diagnosis – Tzanck smear – scrape base of the lesion, Pap smear or biopsy, Cowdry A inclusions, multinucleated giant cells

Question 22

Herpes Beta HHV-5

Answer 22

HHV-5 – CMV, most common TORCH virus, causes mono or asymptomatic in healthy people
Latency – monocytes, lymphocytes

Question 23

Gamma:

Answer 23

HHV-4 – EBV
Latency – B cells – mutations and neoplasm (Burkitt lymphoma), latency 3
Pathogenesis – saliva → oropharynx B cells (sore throat) → ↑ B cells (heterophile Ab=Monospot) → T cell activation (Downey cells) → swelling of spleen and malaise

Question 24

Herpes Beta:

HHV-5

Answer 24

CMV inclusion disease – congenital infection, 2nd most common cause of mental handicap → microcephaly, MR, deafness, blindness, seizures
CMV retinitis – more common with AIDS pts
CMV pneumonia – more common with bone marrow transplant pts

Question 25

Herpes Beta: HHV-6

Answer 25

HHV-6 – roseola infantum (short-lived rash), febrile convulsions, meningitis, encephalitis
Latency – T cells and monocytes
Pathogenesis – replicates in salivary glands, most people are seropositive by adulthood

Question 26

Herpes Gamma:

HHV-4 – EBV

Answer 26

Latency – B cells – mutations and neoplasm (Burkitt lymphoma), latency 3
Pathogenesis – saliva → oropharynx B cells (sore throat) → ↑ B cells (heterophile Ab=Monospot) → T cell activation (Downey cells) → swelling of spleen and malaise

Question 27

Gamma:

HHV-4 – EBV

Answer 27

Infectious mononucleosis – adolescents, high fever, fatige, L+, splenomegaly, sore throat, Downey lymphocytes
Burkitt lymphoma – t8;14 → c-myc activation, endemic along equator, high DNA mutation with EBV
Hodgkin lymphoma – adults, 30% are associated with EBV
Nasopharyngeal carcinoma – adults, derived from epithelial cells
Hairy oral leukoplakia – white plaques don’t scrape off, AIDS pts

Question 28

Herpes Gamma: HHV-8

Answer 28

HHV-8 – Kaposi sarcoma, Primary effusion lymphoma, Castleman’s disease
Latency – B cells, endothelium, monocytes, sensory nerves

Question 29

Herpes Gamma: HHV-8

Answer 29

Kaposi sarcoma –
Classical – Europe and US - raised, purple lesions on the skin
African aggressive – endemic form, rapidly fatal
AIDS related – most common malignancy in HIV/AIDS