Herpes Flashcards
(41 cards)
Pathogenesis of VZV
infection, incubation, replication, spread and reactivation/ secondary infection
what happens after primary infection of VZV?
- Virus remain latent in dorsal root gangly
- later in life, after 60, virus is reactivated and risk increases with age.
- onset of shingle more common AND severe in immunocompromised
- VZV vaccine available for 50+ y/o to prevent shingle
According to the CDC, what precautionary measures should you take to prevent spreadingVZV?
- Keep rash covered
- don’t touch or scratch
- Frequent hand washing
- until rash develops crust, avoid contact with pregnant women you have never had chicken pox or varicella vaccine, premature or low birth weight babies, and/or immunocompromised patients
CMV
infection
Infection is usually through mom to fetus or newborn. also get via sex in adulthood.
usually only a problem for immunosuppressed or very young
neonate contract by transplacental transmission, intrauterine, and/or cervical secretions
baby/child contracts by breast milk, saliva, tears, and/or urine
adult contracts by sexual transmission (semen), blood transaction, or bone graft
causes mental retardation, deafness, neuropathy, pneumonia, retinitis and microcephaly
CMV
cytomegalovirus (HSV-5).
most are infected by middle adulthood
primary infection can result in mono like symptoms
may account for 1/5 of “mono” cases
most common viral congenital infection
4000/yr show symptoms of in utero infection
CMV latency
Established latent infection in many cells, including immune cells- lymphocytes and macrophages.
Virus can be shed in saliva due to chronic replication in salivary glands, for month and even up to 2 years after acute infection
CMV and the immune system
CMV is held in check by our immune system unless there is immunosuppression.
i.e. HIV infection- CMV is the leading cause of death
People on immunosuppressant and receiving organ transplants
EBV
Epstein Barr (HSV-4)
causes most infection cases of mono (79%)
common infection worldwide
frequently seen in high school and college students
“kissing disease”
most people become infected at some point in life
in developing areas in Africa, EBV infection is associated with Burkett’s lymphoma and nasopharyngeal carcinoma
what is infected in EBV?
infection of anti-body producing B cells and makes them hyperproliferate
the infected cells will produce IgM which is detected in the blood (heterophiles lab)
elicit T cell responses that are against the B cells. this causes spleen inflammation and fatigue
Mononucleosis symtoms
Caused by an aggressive T cell response due to the infection and hyper proliferation of the infected B cells
- sore throat
- fever
- swollen lymph glands
- malaise
- sometimes an enlarged spleen or liver
- heart problems (rare)
- CNS problems (rare)
symptoms usually resolve within 1-2 months
remains latent in the throat and blood for the rest of a person’s life
Diagnosis of EBV
patient feels like they have mono
elevated mononuclear WBC count
Heterophiles Ab test: the antibodies that bind non-EBV antigens but are induced by EBV infection.
Staining of cells for viral antigens.
N.B. if a patient has hairy leukoplakia, there is a loss of cytotoxic T cell responses to EBV which leads to a viral re-emergence
Differential Diagnosis between EBV and CMV
CMV is a heterophile negative cause of infectious mono that is most likely confused with EBV infectious mono but usually not accompanied by posterior cervical adenopathy
the CMV infection mono is characterized by its prolonged course of prominent liver involvement.
HHV-6
spread by saliva
present in nearly everyone by adulthood
associated with various neurological problems like MS
possible molecular mimicry of myelin basic protein may stimulate T cell responses that destroy neuron function
Roseola/Exanthema subitum (aka 6th disease) is a rash condition usually occurring in children. Roseola also seen in HHV-7
seems to be linked to Alzheimer’s and infertility
HHV-8
aka Kaposi’s sarcoma associated herpesvirus (KSHV)
causes Kaposi’s sarkoms in people with AIDS
most likely requires immunosuppression
inactivates Rb
HIV Tat protein contributes to development of KS
Formerly a rare cancer found almost exclusively in Mediterranean and sub-Saharan men
HSV-1 HSV-2 VZV EBV (H)CMV HHV-6 HHV-7 HHV-8
herpes simplex virus 1 herpes simplex virus 2 varicella zoster virus Epstein-Barr Virus human cytomegalovirus Human herpes virus 6 human herpes virus 7 human herpes virus 8 aka Kaposi's Sarcoma virus
how does the herpetic lesion spread?
“creep or crawl”
got it’s names from the way it spreads
how long has herpes virus been around
centuries
one of the most common viruses found in humans
Herpes infection
once an individual has become infected it will remain in the body FOR LIFE
it isn’t always active- it can establish a latent state in an immunocompetent host
herpes structure
enveloped icosohedral capsid/ nucleocapsid dsDNA linear (125-230 kb) pleomorphic tegument
Tegument
in herpes, the tegument is between the envelope and capsid. it contains viral protein that assist viral replication
herpesvirus replication
infect non-replicating cells like neurons
it will replicate in the cell’s nucleus
transcription of viral genome by cellular DNA-dependent RNA polymerase
regulated by viral-encoded and cellular nuclear factors
this interplay will determine is the virus is active or latent
encode their own DNA polymerase and thymidine kinase
what happens when infection is symptomatic?
HSV and VZV replicate in a lytic manner. that is, the cells die and then skin lesions form
what happens when the infection is latent?
it is in specific cells types
only a small number of viral genes are expressed
it can then be reactivated
in latency, the immune system cannot see the virus if noRNA or proteins are being made
what happens when the virus is reactivated
reactivation and visions made
lytic replication results with attendant symptoms
