Herpesvirus & Papillomavirus Flashcards
what are some key characteristics of alphaherpesviruses?
- variable host range
- short reproduction cycle
- rapid spread in culture
- efficient destruction of infected cells
- capacity to establish latency in sensory ganglia
HSV-1 infects where? HsV-2?
1: above the waist
2: below the waist
how is HSV-1 spread?
oral-oral or oral genital
how is HSV-2 spread?
primarily genital-genital, oral-genital also possible
where do alphaherpesviruses infect?
epithelial cells in the skin or mucosa; mucosa more susceptible
what is the incubation period for HSV-1/2?
2-14 days but typically 4-5
what are the symptoms of HSV1/2 infection?
flu-like, including localized lesions
only 1/3 show symptoms
lasts for 8 to 12 days
describe the latency assoc with HSV1/2
- stationary cells, genome circularizes and stays as an episome in the nucleus
- peripheral ganglia common site of latent infections
- triggered by sunburn, systemic infection, immune impairment, stress
what is required for alphaherpesvirus to be overcome?
cell mediated immune response
- people unable to produce antibodies can still handle herpesvirus infections
- T lymphocytes detect antigens presented by MHC class I or II proteins
what does herpesvirus do to the immune response?
modulation of immune response
- viral proteins bind antibodies and complement proteins
- counter effects of interferon
how are alphaherpeviruses prevented?
avoid contact during active herpes recurrance
how are alphaherpesviruses treated?
acyclovir limits virus replication but will no eliminate latent infections
what are the key characteristics of betaherpesviruses?
- restricted host range
- long reproductive cycle
- slow progression in cell culture
- enlargement of infected cells (cytomeglia)
- carrier cultures
- latent infection in a variety of tissues
- prototypical member: cytomegalovirus (CMV)
what are the key characteristics of gammaherpesviruses?
- restricted host range
- targets T & B lymphocytes
- lytic infections
- latency in lymphoid tissues
- prototypical member: epstein barr virus (EBV)
what is Burkett’s lymphoma?
- most common childhood cancer in equatorial Africa
- tumor in jaw, eye socket, ovaries
- in all cases, tumor cells have monoclonal EBV episome
- role of EBV still not understood:
- spur B cell growth, mutations or
- genes transform cells
what is Hodgkin’s lymphoma?
- 3 types:
- NL:nodular sclerosing
- MC:mixed cellularity
- LD:lymphocytes depleted
** EBV present in 60-90% of MC & LD tumors, 20-40% of NL tumors
what are the immune evasion antiviral host responses for beta/gammaherpesviruses?
- intrinsic
- innate
- adaptive
where does CMV persist?
in hematopoietic progenitor cells and macrophages in vitro
is there latency with CMV?
no just chronic persistent infection
how is CMV controlled?
by healthy, active immune system
where does EBV persist?
in memory B cells
virus proteins ensure B cell proliferation and EBV genome replication
how are beta/gammaherpesviruses treated and/or prevented?
- infections are usually self limiting in immune competent individuals
- antiviral therapy to inhibit viral genome replication, resistance can develop, and less effective at treating EBV
what is the importance of immunoprophylaxis with CMV?
passive transfer of antibodies for prevention of CMV infection, transfer of EBV-specific T lymphocytes
are there any vaccines for beta/gammaherpesviruses?
no
what kind of virus is human papillmavirus?
- papillomaviridae
- genome: circular dsDNA
- virion: non-enveloped
- proteins:
- L1-cell attachment
- L2-membrane penetration
T/F: plantars/palmars warts are human papillomavirus infections
T
how does human papillomavirus enter the body and cell?
- gain access thru abrasion of skin
- est. infection in basal layer
- cell pol required for genome replication
- virus production in differentiating cells
- non-lytic, virus released with dead cell shedding
how is human papillomavirus infection acquired?
- direct skin-to-skin contact, fomites
- normal skin is very strong barrier
- mucous membranes more susceptible
- virus enters body thru abrasions
- virus is hardy to environ. stresses; allows transmission via fomites
what are the symptoms of human papillomavirus infection?
- site of infection
- take months to manifest
- warts- raised or flat-~50% regress on their own in 2 years
what is respiratory papillomatosis?
rare complication, respired virus, can be lethal
how does oncogenesis - cervical cancer occur in human papillomavirus?
- HPV requires actively replicating cells to replicate and produce progeny
- E7 blocks retinoblastoma (Rb) protein- continued cell proliferation
- E6 blocks the p53 suppressor pathway
- actual path to cancer unknown: viral transformation, cell proliferation leading to cancerous mutation
how is human papillomavirus treated and prevented?
- most treatments ablative: liquid nitrogen, surgical excision, laser, caustic chemicals
- no proof that condoms reduce risk
- vaccination: Gardasil
