UGI 5 Flashcards
most herpes are what strain
HHV-2/HSV-2
when are the viruses HHV-1/2 typically released
released from the genital ulcers and in between outbreaks from the skin
although herpes is usually asymptomatic, what is the primary symptom
1+ blisters around the genitals or the rectum
which outbreak of herpes is the worst and what triggers the virus
the first outbreak is the most severe and subsequent outbreaks after decrease over time
triggered by stress, UV light from the sun, low immune system
what does HHV-1 and 2 share?
DNA homology, antigenic determinants, tissue tropism, disease symptoms
describe the HHV-1 and 2 virus?
ubiquitous, large, ds DNA, enveloped icosahedral virus that stays indefinitely in the body
what do HHV-1 and 2 encode and why it is important
enzymes that are good as anti viral targets
types of cells that HHV-1 and 2 infect and replicate in
mucoepithelial cells
pathogenesis of herpes virus and cells that fall under each one
lytic - cowdry type A inclusion bodies, syncytia
persistent - lymphocytes and macrophages
latent - neurons
how does the herpes virus protect itself from getting killed
- blocks effects of interferons
- prevents CD8 T cell recognition of infected cells
- escapes antibody neutralization and clearance by going into hiding during latent phase
how do you diagnose herpes
PCR or serological tests
how do you diagnose herpes in between outbreaks
blood tests to detect antibodies (not always definitive)
how do you treat herpes
there is no cure but you can treat with acyclovir, famciclovir, valacyclovir
how does one reduce transmission of herpes
daily suppressive therapy
how does acyclovir work
- it is a guanine analogue that uses thymidine kinase for phosphorylation and gets incorporated onto the DNA strand
- acyclovir triphosphate blocks DNA synthesis because once incorporated, there is chain termination due to lack of 3’ OH
microbe involved in donovanosis/ granuloma inguinale
klebsiella granulomatis
describe klebsiella granulomatis
gram neg rod surrounded by well defined bipolar staining capsule, pleomorphic, intracellular, microscopy safety pin appearance with stain
how does donovanosis/granuloma inguinale present
- painless slow growing ulcerative lesion on genital or perineum without regional lympadenopathy
- highly vascular hence reason for beefy red appearance and it bleeds easily on contact
extragenital infections of donovanosis/granuloma inguinale
pelvis, dissemination to intra-abdominal organs, bones, mouth
high risk and low risk strand for HPV
high risk - HPV 16, 18
low risk - HPV 6, 11
spectrum of HPV associated diseases
- cervical dysplasia and cancer
- condyloma acuminata (genital warts)
- other anogenital and oral cancers
anogenital warts caused HPV are usually asymptomatic but what happens if it goes untreated
may increase in size or numbers
how do you diagnose anogenital warts
visual inspection
what poses a greater risk in contracting cancer than alcohol and smoking? what evidence supports it?
HPV
HPV 16 is present in 72% of patients with cancer
what has decreased the rates of cervical cancer
pap smear
strand of HPV present in cervical cancers
HPV 16, 18
describe HPV genome
circular, dsDNA
what types of cells do HPV infects
infect epithelial cells
what does HPV E6 and E7 bind and what does it do
p53 and Rb respectively and disrupts the cell growth cycle
what is the HPV lifecycle tight coupled to
differentiation process of the epithelium
how do you diagnose cervical cellular abnormalities
- cytology/pap test for screening
- HPV DNA tests
- colposcopy
- cervical biopsy
how often do women 21-29 and 30-65 get tested for cervical cell abnormalities and what tests are done
- -> 21-29: pap test every 3 years
- –> 30-65: pap test and HPV every 5 years or pap test alone every 3 years
HPV vaccine and strands it protects against
- Gardasil: 6, 11, 16, 18
- Cervarix: 16 and 18