Viral Infections Flashcards
Herpes simplex viruses
Establish latent infections that persist for the life of the individual
Two types -
HSV1: stomatitis (cold sore). Infection via mouth/skin producing an inflammatory reaction and ulcers. Virus establishes latency in trigemial ganglia, reactivates by stress, trauma, febrile illness. Produces localised lesion.
HSV-2 (genital warts). Virus establishes latency in sacral ganglia. Primary infection presents with fever, myalgia and painful shallow ulcers.
Varicella zoster virus
Produces chicken pox (primary) and shingles (reactivation).
Primary infection occurs via aerosolised drops or directly from vesicle fluid. Fever and malaise precede rash.
Infectious period from 2 days before rash until crusting stage. Following recovery the virus establishes latency in dorsal root ganglion.
Reactivation occurs in dermatome distribution of the sensory nerve. Severe pain.
Progression of chickenpox rash
Macula
Papule
Fluid filled vesicle
Crusting
Rash appears in crops
Complications of chicken pox
Infected lesions - GA Strep in children
Pneumonia in immunosuppressed, pregnant, smokers. Diffuse infiltrates seen on CXR.
Prevention of chicken pox
Live attenuated vaccine
VZV IgG
Prophylactic acyclovir
When would it be appropriate to intervene in a patient with suspected chicken pox?
Consider: susceptibility - previous exposure, VZV IgG protective
Risk of severe disease - immunosuppressed or pregnant
Significant exposure
Give VZV IgG within 10 days of contact
Acyclovir if contact develops breakthrough infection
Infectious mononucleosis
Glandular fever - fever, pharyngitis, lymphadenopathy possible splenomegaly
caused by EBV mostly (CMV or primary HIV)
EBV establishes latent infection in B cells, major agent responsible for Burkitts lymphoma.
Diagnosis can be made clinically. Tests done if you suspect atypical cause.
Influenza infection
Acute respiratory infection - fever, sore throat, myalgia, headache
Contagious and changing due to antigenic drift. Pandemics caused by antigenic shift.
Complications - pneumonia (viral/bacterial) or hepatitis
Treat with neuraminidase inhibitors
Influenza prevention
Vaccine (seasonal)
Prophylactic antivirals
Children, elderly, chronic disease, pregnancy and high BMI patients most at risk.
AIDS
Combination of signs and symptoms caused by HIV infection
Progressive loss of CD4+ cells leads to immunodeficiency
Results in unusual opportunistic infections, AIDS related cancers.
Transmission of HIV
Sexual (anal, vaginal, oral Increased presence of STIs Vertical >30% Intravenous drug use Transfusion and blood products
Highest risk of HIV transmission following exposure from HIV individual
Anal intercourse
Needle stick injury
Shared needles
Target cells for HIV replication
CD4+ T cells
Macrophages
Microglia
Dendritic cells capture the virus and pass it onto CD4 cells. Infected CD4 T cells are the main source of an HIV infected individual
Describe natural course of HIV infection
CD4 T cells 600-1600 cells/ml in an immunocompetent individual.
Following infection, there is a transient fall in CD4 as the HIV virus peaks, there is then a decrease in viral load. This takes approximately 3 months. Time between infection and initial peak is the window period.
Between 6 months - 10 years the virus slowly replicates and CD4 cell count slowly declines (relative latency). Patients are asymptomatic
Once CD4 cells have declined below 350 cells/ml patients present with symptoms and there is rapid production of virus.
Speed of the progression of AIDS is dependent of viral load
Briefly describe the lifecycle of HIV
The human immune deficiency virus binds to host CD4 molecules via an envelope glycoprotein. Binding to secondary receptors (chemokine receptors CCR5, CXCR4) is required for entry, conformational change results in fusion with the cell membrane.
Entry of the viral capsid is followed by uncoating of RNA. DNA copies are made from both RNA templates (reverse transcriptase). The enzyme DNA polymerase from the host cell leads to formation of dsDNA.
In the nucleus the virally encoded DNA is inserted into the host genome (integration). Regulatory proteins control transcription. The virus is reassembled in the cytoplasm and budded out from the host cell.
