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Flashcards in Viral Infections Deck (20):

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

Fluid filled vesicle

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
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.



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

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.


Anti-retroviral drugs

Target replicating virus (mainly directed at viral enzymes).

Nucleoside analogues (NRTIs)
Protease inhibitors
Non-nucleoside analodues NNRTIs
Integrase inhibitors
Fusion inhibitors

Drugs used in combination - 3 drugs from two classes. Reduces the risk of resistance

Normally start with 2 NRTIs and 1 NNRTI

Treatment life long and expensive


Interventions to prevent vertical transmission of HIV

Antiretroviral therapy for mother
Formula feeding
Treatment for neonate for 6 weeks

Reduces risk from 30% to <0.1%


Significance of latency in HIV infection

Non-proliferating cells are latently infected (secondary sites) e.g. ovary, prostate, testis. Following treatment with HAART the viral load is reduced, however it cannot act on latent virus. If therapy stops, the latent virus reactivates.

Compliance with treatment is important


AIDS-defining illnesses

Karposi's sarcoma - if only on the skin, it responds well to HAART but can invade internal organs, requires chemotherapy

Toxoplasmosis - infection causes acute inflammatory lesion of the retina which leaves retinal scarring. Eye pain, photophobia, blurred vision. Can reactivate.


Pneumocystis pneumonia - Occurs when CD4 count falls below 200, causes respiratory failure. CXR shows diffuse bilateral shadowing with butterfly pattern (pneumonia normally consolidated)

Candidiasis: only when affecting viscera e.g. oesophagus

Cancers: viral origin mostly. Unable to clear cells transformed by virus.


Name two viral causes of arthritis


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