Blood borne viruses

Question 1

What are blood borne viruses?

Answer 1

Viruses with a viraemic phase that may be self-limited (acute with recovery) or persistent (chronic)

Question 2

What’s the virology of Hep B?

Answer 2

 Hepadnaviridae
 Enveloped virus
 Double stranded DNA genome

Question 3

What are the clinical features of Hep.B?

Answer 3

 Incubation period average 60-90 days (45-180)
 ACUTE INFECTION
 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
 CHRONIC INFECTION
 May see signs of chronic liver disease
 Chronic infection: 5 yrs, 2%-10%

Question 4

What’s the burden of chronic Hep B infection?

Answer 4

 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)

Question 5

What’s the management of acute hepB?

Answer 5

 Supportive, antivirals not given
 Counsel regarding transmission
 Screen for other bloodborne viruses, STDs
 Notifiable disease  Trace, test, and immunise relevant contacts

Question 6

What’s the management of chronic Hep B?

Answer 6

 Defined as on-going infection for >6 months

 If ALT/ HBV viral load/ liver biopsy suggest risk of progression- antiviral therapy

Question 7

What’s Hep B antiviral therapy?

Answer 7

 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

Question 8

How can you prevent Hep B infection?

Answer 8

 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

Question 9

What’s the virology of Hep C?

Answer 9

 Flavivirus, Hepacivirus, 1989
 Positive single stranded RNA
 Enveloped
 Many different genotypes distributed geographically

Question 10

What’s the natural history of Hep C?

Answer 10

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%)

Question 11

What’s the burden of Hep C?

Answer 11

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

Question 12

How can you diagnose Hep C?

Answer 12

 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

Question 13

How can you manage acute Hep C?

Answer 13

 Difficult to spot-usually asymptomatic
 High dose interferon alpha clears infection in most people
 Notifiable to public helath

Question 14

How can you manage chronic Hep C?

Answer 14

 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

Question 15

How can you prevent Hep C?

Answer 15

 No vaccine
 Risk reduction and counselling  E.g. needle exchanges
 Screen and test donors  Virus inactivation of plasma-derived
products
 Safe injection and infection control practices

Question 16

What is the virology of Human Immunodeficiency Virus (HIV)?

Answer 16

Retrovirus
•Lentivirus
•Enveloped
•Diploid RNA genome

Question 17

What’s the origin of HIV?

Answer 17

• 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

Question 18

What’s the risk of HIV transmission?

Answer 18

 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%)
&raquo_space;Variable according to viral load in genital tract, breeches in mucosal barrier, other STI (HSV)

Question 19

How can you diagnose HIV?

Answer 19

 First antibody tests developed 1985 (blood screening)
 Screen/ test • Risk groups, in pregnancy, contacts, or investigation
of illness
 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

Question 20

What’s the pathogenesis of HIV?

Answer 20

 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

Question 21

What’s the clinical progression of HIV?

Answer 21

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.

Question 22

What is Kaposi’s sarcoma?

Answer 22

An opportunistic infection.
Characteristic raised purple lesions occur anywhere throughout body
Associated with HHV8 infection Rare now in the era of HIV therapy

Question 23

What’s oral hairy leukoplakia?

Answer 23

An opportunistic infection.
Non-painful white plaques along lateral tongue borders
Associated with EBV infection
Correlates with smoking
AIDS defining
Treatment is by improving CD4 count

Question 24

What’s the management of HIV?

Answer 24

 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

Question 25

What’s combination therapy?

Answer 25

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)

Question 26

What’s the practice for needlestick injuries?

Answer 26

 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%

Question 27

How should you manage a significant needlestick injury?

Answer 27

 If significant event
 Prophylaxis- HBV vaccine/ HBIG
 HIV PEP
 Follow up and early treatment for HCV
 Storage sample (prove not already infected)
 Managed by occupational health