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24 Cards in this Set

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Human T Cell Leukemia Virus Type I - HTLV-I Viral Properties and Replication
- causes adult T cell leukemia (ATL) - envelope – one of its glycoproteins does entry into the cell – target for neutralizing Abs - carries several viral enzymes for replication
HTLV-I Retroviruses
- formerly called RNA tumor viruses - have RT and RNase H to copy RNA into DNA intermediate - integrase inserting viral DNA into the host chromosome - large precursor proteins assemble the particle then are cleaved by protease
HTLV-I Clinical Features
- low virus load w/ seroconversion shortly after infection - malignant infected cells are mature T cells, w/ multilobed nucleus - characterized by high WBCs, infiltration of CNS and rapidly fatal course - can cause immunodeficiency, leading to opportunistic infections
HTLV-I Pathogenesis
- act as a cofactor in tumor formation - first there is transient polyclonal outgrowth of cells w/ integrated DNA - inappropriate expansion may allow other genetic changes - viral expression is difficult to detect, which suggests that viral gene product is not required to maintain the transformed state and its role is early - if virus-encoded tax transcriptional activator protein increased the expression of IL2 and its receptor, cell growth would be chronically stimulated – window for genetic mutations that contribute to cell growth and malignancy - associated w/ p53 mutation and tropical spastic paraparesis (TSP), a myelopathy – SC inflame that leads to partial paralysis
HTLV-I Treatment
- no treatment for 1o (usually inapparent) - chemo leads to short term remission in 50%
HTLV-I Epidemiology
- via semen, milk, and blood - Male to female common, female to male rare - Vertical (via breast feeding) is the main means - low lifetime risk if infected of developing ATL or TSP - very low level throughout the world
HTLV-I Prevention
- Vaccination of women would work - donated blood is screened
Human Papilloma Virus - HPV Properties and Replication
- naked, papovavirus family – circular dsDNA - 70 strains w/ strict epithelial cell tropism
Human Papilloma Virus - HPV Clinical Features and Pathogenesis
- cause epithelial dysplasias (i.e., warts) - via viral contact with MMs or traumatized skin - some cause common warts, others associated w/ carcinomas - in the cancers the viral genome is frequently integrated breaking the circular DNA so that an important viral regulatory protein is not produced -> viral genes E6 and E7 to be produced at a higher level -> inactivating the cell’s tumor repressor genes, Rb and p53
Human Papilloma Virus - HPV Diagnosis
- find cervical dysplasia in paps - PCR to identify a specific strain
Human Papilloma Virus - HPV Epidemiology
- via direct contact - more common in older children and young adults - not highly contagious, epidemics are rare, but genital warts #1 STD (w/ Chlamydia) - 2-6 month incubation - cervical cancer is 1/4 of all cancer in women - some genital tract HPVs (including the squamous cell cervix carcinoma one) are considered STDs – high # of sexual partners is main RF
Human Papilloma Virus - HPV Prevention and Treatment
- Limiting # of sexual contacts and do regular Paps - 50% of common skin warts will regress spontaneously - can do surgical removal, but reoccurrence is common
Epstein Barr Virus Properties and Replication
- herpesvirus that gets 90% of the world pop - linked to B-cell and epithelial malignancies - can infect B’s in vitro and induce growth in culture - most cell lines from PBL don’t produce infectious virus – considered “latently” infected - In nucleus, linear DNA forms the extrachromosomal episome - replicated by host and partitioned to each daughter cell (as long as oriP and EBNA1 are there)
Epstein Barr Virus Clinical Features and Pathogenesis
- 1o usually early in life, frequently by age 3 - largely asymptomatic - IM, BL, NPC, HD
EBV Infectious Mononucleosis (IM)
- salivary exchange, then replicates in epi (tonsillar lymphocytes?) -> viremia - 1st wk - portion of circulating Bs are EBNA (+) and may produce IG and autoantibodies (the heterophile Ab reacts w/ sheeps blood and is used to diagnose) - imbalance between a polyclonal proliferating and latently-infected B’s VS cytotoxic T’s that would control them - then there is latent infection in B’s (escapes the cytotoxic Ts) - virus DNA persists as episome and infection persists for life - degree shedding varies – may reflect a chronic low grade replication in OP epi cells
EBV Burkitt’s Lymphoma (BL)
- endemic area in Africa, tumors in jaw - kids before two years - characteristic chromosomal translocation that alters the regulation of c-myc expression so its controlled by IG promoters - elevated Ab titers to viral Ags, like VCA and EA, preceding the tumor - All tumors have EBV in all of the malignant cells
EBV Nasopharyngeal carcinoma (NPC)
- epithelial tumor - in Asia - elevated Ab titers to viral Ags - viral genome in malignant cells - other co-factors contribute to cancer development - latent infection then expression of viraltransforming genes are crucial events
EBV Hodgkin’s disease (HD)
- if history if IM, 2 to 4X more likely to get this lymphoma which develops from EBV infected cells - Reed-Sternberg cell (similar to those in IM) is malignant cell - viral DNA and EBERs commonly found in RS cells
EBV Lymphoma associated with immunosuppression
- may develop in patients with congenital immune impairment - also responsible for most post-transplant lymphoma (PTL)
EBV Diagnosis
- IM is characterized mononucleosis (atypical lymphocytosis) and “monospot” test (sheep blood thing) - malignancies identified clinically in high risk populations - BL or NPC have serologic responses prior to onset of malignancy
EBV Treatment and Prevention
- latent infections, so antiviral therapy for the viral DNA polys wont work - IM self-limiting, symptoms vary widely - no vaccine (it would eliminate ass. Cancers) - Post-transplant lymphoma treated by reducing immunosuppression and by giving viral-specific cytotoxic lymphocytes - in cancers, multiple viral proteins for weird growth so immune-mediated therapy and specific molecular therapy directed toward the viral functions will work
Human Herpes Virus 8 (HHV-8) Virus Properties and Replication
- most recently discovered HHV, discovered in Kaposi’s sarcoma (KS) - in transformed cell, viral DNA is circular, possibly clonal - has genes acquired from the host genome - may induce growth by inducing infiltrating cells to secrete cytokines or by expressing autocrine growth stimulatory molecules
Human Herpes Virus 8 (HHV-8) Clinical Features and Pathogenesis
- KS not very aggressive - forms multiple skin lesions - incidence has dramatically increased in HIV patients - caused by a STD agent, with patterns of appearance, remission, reactivation seen in other herpesviruses
Human Herpes Virus 8 (HHV-8) Epidemiology
- consistently detected in AIDS-associated as well as classical KS - rarely detected in normal healthy subjects - sometimes in AIDS lymphomas - may not be ubiquitous