Flashcards in Blood borne viruses Deck (27)
What are blood borne viruses?
Viruses with a viraemic phase that may be self-limited (acute with recovery) or persistent (chronic)
What's the virology of Hep B?
Double stranded DNA genome
What are the clinical features of Hep.B?
Incubation period average 60-90 days (45-180)
Virtually all infants and children asymptomatic, up to 50% adults asymptomatic, especially likely if HIV infected
Acute case-fatality rate: 0.5%-1% If symptomatic, prodrome, icteric phase
May see signs of chronic liver disease
Chronic infection: 5 yrs, 2%-10%
What's the burden of chronic Hep B infection?
Premature mortality from cirrhosis and HCC 15%-25%
Worldwide HBV infection accounts for 30% of all cases of cirrhosis and 53% of all HCC cases (lower for UK)
What's the management of acute hepB?
Supportive, antivirals not given
Counsel regarding transmission
Screen for other bloodborne viruses, STDs
Notifiable disease Trace, test, and immunise relevant contacts
What's the management of chronic Hep B?
Defined as on-going infection for >6 months
If ALT/ HBV viral load/ liver biopsy suggest risk of progression- antiviral therapy
What's Hep B antiviral therapy?
Nucleoside analogues Lamivudine, adefovir, entecavir,
tenofovir Effective rapid reduction in HBV DNA Antiviral resistance may develop Prolonged or life long therapy
Immunomodulators Interferon alpha (pegylated) Response rate 60% at best Side effects
How can you prevent Hep B infection?
Avoid or reduce risk • Safe sex, needle exchange, infection control
Screening • Blood products, risk groups, pregnancy
Vaccine Safe, recombinant sAg Primary prevention, post exposure Active or passive (HBIG) Know your status
What's the virology of Hep C?
Flavivirus, Hepacivirus, 1989
Positive single stranded RNA
Many different genotypes distributed geographically
What's the natural history of Hep C?
1. Incubation period 6-8 weeks
2. Acute Hep C
3. Develops to chronic Hep C (85%)
4. Cirrhosis (20%)
5. Liver cancer, liver failure (25%)
What's the burden of Hep C?
Worldwide HCV infection accounts for 27% of all cases of cirrhosis and 25% HCC
HCV infection is now the major indication for liver transplant in USA and Europe
How can you diagnose Hep C?
Usually picked up by screening risk groups or contacts or as part of liver disease work up
Antibody or nucleic acid (RNA)
Seroconversion window period
Some patients never make detectable antibody, esp. immunosuppressed
How can you manage acute Hep C?
Difficult to spot-usually asymptomatic
High dose interferon alpha clears infection in most people
Notifiable to public helath
How can you manage chronic Hep C?
Assessment LFT, symptoms, liver biopsy or
fibroscan to measure severity
Immunise against HAV, HBV
Antiviral therapy to clear virus and prevent progression
Combination antiviral therapy
Pegylated interferon and ribavirin can clear virus in up to 80% non-genotype 1, and 50% genotype 1
Side effects and adherence
Promising new agents-protease, polymerase inhibitors
How can you prevent Hep C?
Risk reduction and counselling E.g. needle exchanges
Screen and test donors Virus inactivation of plasma-derived
Safe injection and infection control practices
What is the virology of Human Immunodeficiency Virus (HIV)?
•Diploid RNA genome
What's the origin of HIV?
• HIV (or similar) antibody found in sera from Zaire 1959
• HIV1 related to chimpanzee virus
• Evidence of spread among gay American males from 1977
• HIV2 related to virus found in Sooty Mangabey
• Human epidemic probably result of exposure to blood during animal butchering, spread occurring via urbanisation in 1950’s and international travel from 1970’s
What's the risk of HIV transmission?
From known HIV infected individual:
Blood transfusion (one unit) Receptive anal intercourse Receptive vaginal intercourse Insertive vaginal intercourse Insertive anal intercourse
Receptive oral sex (fellatio) Needle–stick injury Sharing injecting equipment Mucous membrane exposure
90-100% 0.1-3.0% 0.1-0.2% 0.03-0.09% 0.06% 0-0.04% 0.3% (95% CI 0.2%-0.5%) 0.67%
0.09% (95% CI 0.006%-0.5%)
>>Variable according to viral load in genital tract, breeches in mucosal barrier, other STI (HSV)
How can you diagnose HIV?
First antibody tests developed 1985 (blood screening)
Screen/ test • Risk groups, in pregnancy, contacts, or investigation
Sensitivity increased by use of ‘dual’ assays
• Detect virus antigen and antibody- 4th generation tests
• Reducesseroconversionwindowperiod-timefrom infection to being antibody positive
Detection of virus genome (viral load) may reduce window further
What's the pathogenesis of HIV?
HIV infects CD4 positive cells
T cells, macrophages, dendritic cells, microglia
CD4 cell turnover 108-9 cells/day Virus production up to 1010/day Immune cell production cannot ‘keep up’ Immunodeficiency results
Virus escapes full immune control • High turnover and mutation rate of envelope antigen target • Integrated into dormant cell genome
• Interference with immune function signalling
What's the clinical progression of HIV?
1. Acute retroviral syndrome, oral or oesophageal candidiasis.
2. Herpes zoster (shingles), vaginal candidiasis
3. Oral oesophageal candidasis, Kaposi's sarcoma, TB
4. Pneumocystosis, cryptococcosis, histoplasmosis
5. Resistant candidiasis, CMV disease, MAC disease.
What is Kaposi's sarcoma?
An opportunistic infection.
Characteristic raised purple lesions occur anywhere throughout body
Associated with HHV8 infection Rare now in the era of HIV therapy
What's oral hairy leukoplakia?
An opportunistic infection.
Non-painful white plaques along lateral tongue borders
Associated with EBV infection
Correlates with smoking
Treatment is by improving CD4 count
What's the management of HIV?
Investigate for other infections, assess general health, counsel regarding transmission
Assess need for antiretroviral therapy based on symptoms, CD4 count, and viral load
Not everyone needs ART (antiretroviral therapy) at the time of diagnosis
Balance side effects and drug resistance with protection against immune deficiency
What's combination therapy?
Standard of care is currently to use HAART (highly active antiretroviral therapy)
Multiclass combination therapy
o More potent
o Less risk drug resistance
o (more side effects)
What's the practice for needlestick injuries?
Avoid- safe practice First aid Report Risk assess
May not be appropriate for recipient of injury to do
Risk of transmission depends on amount of virus exposed to and pre- existing immunity
Hollow bore/ solid needle; venepuncture/ injection; scratch/deep wound/ mucosal exposure; viral load of source
HBV 30-3%; HCV 1-3%; HIV 0.3%