Blood Borne viral infections by Nsanzimana Jerome Snavy university of Rwanda Biomedical Laboratory sciences departement

1. Group VI
• Members:Group VI
NAMES Reg numbers
1. TWAHIRWA Wellars 218002441
2. NSANZIMANA Jerome 218002673
3. INGABIRE Hosiana 218002348
4. NGABOYIMANA Jean Damascene 218002345

2. BLOOD BORNE VIRAL INFECTION
• Blood borne viruses (BBVs) are viral infections that
can be transmitted from person to person through
blood or body fluids containing viruses.
Transmission routes
• sexual intercourse (common for HBV, HIV; inefficient
for HCV);
• sharing injecting equipment.
• skin puncture by blood-contaminated sharp objects
(e.g. needles, instruments or glass).
• childbirth ( the mother infects the child either
before or during birth, or through breast-feeding)

3. a. Hepatitis B Virus
 HBV is a member of the hepadnavirus family.
Enveloped, icosahedral nucleocapsid core with
partially double-stranded circular DNA genome
Replicate via reverse-transcriptase
 HBsAg: is Hepatitis B surface antigen in capsid.
 HBeAg is seromarker for highly viral replication
 HBcAg major structural protein of nucleocapsid
 HBxAg Potent transactivator of cellular and viral
genes(stimulates cell cycle)

4. Pathogenesis
After entering the blood, the virus infects
hepatocytes, and viral antigens are displayed on the
surface of the cells.
Cytotoxic T cells mediate an immune attack against
the viral antigens on infected hepatocytes ,
inflammation and necrosis occur. Antigen–antibody
complexes cause some of the early symptoms (e.g.,
arthralgia, arthritis, and urticaria) and some of the
complications in chronic hepatitis (e.g.
Glomerulonephritis, cryoglobulinemia, and
vasculitis).

5. • HBV pathogenesis can develop into:
Acute hepatitis: short-lived infection, last less than 6
months.
Fulminant hepatitis: severe acute hepatitis with
rapid destruction of the liver.
Co-infection with hepatitis(D) : HDV infect person
with HBV
Chronic hepatitis:
 Asymptomatic carrier: patient never develops
antibodies against HBsAg and no liver damage.
 Chronic persistence hepatitis: patient has low grade
hepatitis.
 Chronic active hepatitis: patient develops Anti-HBsAg in
blood and has acute hepatitis state which continue
without normal recovery (lasts longer than 6-12
months).

6. Complication
• Primary hepatocellular carcinoma, where HBV DNA
becomes incorporated with hepatocyte DNA (DNA
mutation)and triggers malignant growth.
• Liver Cirrhosis, due to permanent liver scarring and
loss of hepatocytes
Laboratory diagnosis
• Serologic test: detect presence of HBsAg and for
IgM or IgG antibody (Anti-HBc.)

7. • Liver ultrasound. A special ultrasound called transient
electrography can show the amount of liver damage.
• Liver biopsy. Your doctor might remove a small sample of
your liver for testing (liver biopsy) to check for liver
damage.
Disease state HBsAg Anti-
HBsAg
HBeAg Anti-
HBeAg
Anti-
HBcAg
Susceptible - - - - IgM
Immune due to natural
infection
- + - + -
Immune due to
hepatitis b vaccination
- + - - -
Acutely infected + - + - IgM
Chronically infected + - + - IgG

8. Treatment and prevention
Anti-viral medication for treatment of chronic active
or persistence HBV infection. Like entecavir,
tenofovir, lamivudine, adefovir and telbivudine
Interferon injections. Interferon alfa-2b (Intron A)
stimulates immune response , treat cancers.
Liver transplant. If your liver has been severely
damaged, a liver transplant may be an option.
Serologic tests on donor blood to remove HBV
contaminated blood from the donor pool.
Active immunisation

9. b. Hepatitis C Virus
HCV is an enveloped icosahedral with positive-sense
single-stranded RNA flavivirus. HCV is transmitted
parenterally, with primary means of infection being via
injection drug use.
 Pathogenesis
• Hepatitis c virus is able to escape innate and adaptive
immune. Once HCV has settled the hepatocytes, the
outcome of HCV infection is determined by the
interaction between the virus and host immune system.
Multi-specific CD8+T-cell response, along with a
coordinated CD4+T-cells response that is associated
with eradication of the infection.

10. Cont’d
• In most patients, the humoral, cellular immune,
and cytokines response seem insufficient to
eradicate the infection, nonspecific immune
response is amplified so that the body controls
replication of virus. This attempt to clear virus from
the liver cells, the immune response contributes to
hepatocellular damage enhancing liver failure,
cirrhosis and liver cancer.

11.  Diagnosis
Virological diagnosis of HCV infection is based on two
categories of laboratory tests, which are:
• Indirect test by using ELISA Test to detect antibodies
(IgM and IgG) induced by viral infection.
The test does not distinguish between IgM and IgG
and does not distinguish between an acute, chronic,
or resolved infection. Because false-positive results
can occur in the ELISA

12. Direct test to detect viral antigens and viral nucleic
acids by using Recombinant immunoblot assay (RIBA)
should be performed as confirmatory test.
If the results of RIBA are positive, a polymerase chain
reaction–based test that detects the presence of viral
RNA (viral load) in the serum should be performed to
determine whether active disease exists.
 Treatment:
Interferon and ribavirin are the two drugs for chronic
Hepatitis C

13. C. Hepatitis D Virus
It is known as hepatitis Delta virus, it has incomplete RNA
virus, only infect and replicate with help of HBV. HDV
helical nucleocapsid actually use HBV’s envelop, HBsAg.
Can only cause infection with the HBsAg coat.
 Pathogenesis:
Co-infection: HDV and HBV both are transmitted to
gather parenterally. And Cause acute hepatitis similar to
that caused by HBV. Antibodies to HBsAg will be
protective against both, ending the infections.
Superinfection: HDV infect person with chronic HBV
infection. This infection is often severe, with higher
incidence of fulminant hepatitis and cirrhosis. Patient
with chronic HDV can’t make Anti-HBsAg and so remain
chronically infected with HBV and HDV.

14. Cont’d
Diagnosis:
Detection of serum HDAg,
 detection of serum HDV RNA,
detection of anti-HDV antibody,
Tissue markers of HDV infection
Treatment:
No treatment, only control of HBV infection is
currently the only way of to protect against HDV.

15. d. Human Immunodeficiency Virus (HIV)
HIV is single-stranded RNA retrovirus responsible for
causing acquired immunodeficiency syndrome (AIDS).
• There is no cure for HIV but it can be treated. If a
person with HIV does not get treatment for their
condition, HIV can cause AIDS. This means the
person’s immune system has become more
damaged and is no longer able to fight off infections
and cancer.
• It is estimated that about 50,000 people will
contract HIV each year.

16.  Pathogenesis:
• After entry HIV begins replication immediately
resulting in a rapid progression of AIDS or chronic
latent course. This progression occurs in 3stages:
• 1. Acute viral illness characterised by high fever,
malaise, lymphadenopathy, pharyngitis, develops in
80% about one month after initial exposure. There
is high level of HIV in the blood and the virus spread
to infect lymph nodes and macrophages. HIV-
specific immune response arises and resulting in
decreased viremia. However, replication continues
in lymph node and peripheral blood.

17. 2. A clinical latency follows for a median of 8 years with no
symptoms of AIDS, HIV continues its replication in lymphoid
tissue and there is a gradual destruction of CD4+T-cell
lymphocyte (helper) cells.
The virus reproduces in these cells and destroys them.
Toward the end of 8 years the patients are more susceptible
to bacterial and skin infections and develop systemic
symptoms such as fever, weight loss, night sweat and
adenopathy.
3. AIDS develops for a median of 2years followed by death.
Now AIDS is defined as having CD4 +T- lymphocyte count of
less than 200 (with serologic evidence of HIV infection such
as ELISA or western blot test) or one of many AIDS
opportunistic infections develops only in AIDS patients.
Candida esophagitis, pneumocystis carinii pneumonia and
many others.

18.  Clinical course of HIV infection 3 stages:
CD4 T cells decline over time and opportunistic
infections develops at specific CD4 T-cell count.
• Normal CD4 T-cell counts are 1000cells/μl blood. In
HIV infected persons the count decrease about
60cells/ μl blood/year.
• 400-200(about 7 years): patient develops symptoms
such as weight loss, fever, night sweat, adenopathy,
skin infection such as athlete’s foot, oral
brush(candida albicans) , bacterial infection (M.
tuberculosis).

19. Cont’d
•˂ 200 about 8years: as immune system fails,
the serious opportunistic killers set in such as
pneumocystis carinii pneumonia, Cryptococcus
neoformans and T.gondii.
•˂ 50: at this level the immune system is
completely down. Mycobacterium avium-
intracellular, normally causing infection in birds
cause disseminated disease in the AIDs
patient. Also cytomegalovirus rises as count
moves from 50 to zero.

20. Diagnosis:
After infection with HIV, viral RNA or antigens can
be detected in blood within weeks. 3 to 6 weeks
later antibodies against HIV antigen appear.
• ELISA (enzyme linked immunosorbent assay) test
detects antibodies. It is very sensitive at detecting
HIV infection but it is false positive result .
For antibody ELISA, Antigens are stuck onto a
plastic surface and a sample is added then
antibodies for a virus being tested will bind to
antigens. If antibodies are present in sample, a
second added antibody with marker will react
and change color

21. Cont’d
If no antibody, no reaction and color change with the
second antibody with a marker.
For antigen ELISA, antibodies are bound to a plastic
surface, sample is added and if antigens from virus
being tested are present they will stick to antibodies.
• Western blot is performed to confirm positive ELISA.
In this test HIV antigens are separated in bands on
paper by molecular weight. The patient serum is
added to the paper if the serum contains antibodies
against HIV antigens they will stick to antigens on
the paper then anti human antibodies (labelled with
enzymes) are added and sticks to antibodies on
antigens lighting up(band) on the paper.

22.  Control, Treatment and cures:
• Prevention of HIV viral infection.
• Tenofovir (TDF),lamivudine (3TC) or emtricitabine(FTC)
and efavirenz (EFV) recommended by WHO as
antiretroviral drugs.
• Treating the opportunistic infection
• Limiting growth of HIV, once infection has occurred.
Effective treatments are available to manage HIV. The
treatment is generally in the form of a tablet which
needs to be taken daily. HIV can never be completely
cleared from your body, you must take steps to protect
your health and the health of others.

23. References:
1. Mark Gladwin, M.D. and Bill Tattler, M.D. 2011, Clinical
microbiology, 5th, Med Master , Miami
2. Mayo Foundation for Medical Education and Research
2017, treatment for chronic hepatitis B infection, viewed
on 21 march 2019,
<https://www.mayoclinic.org/diseases-
conditions/hepatitis-b/diagnosis-treatment/drc-
20366821
3. Division of Viral Hepatitis, National Center for
HIV/AIDS, Viral Hepatitis, STD, and TB Prevention,
Interpretation of Hepatitis B Serologic Test Results,
www.cdc.gov/hepatitis
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC44502
01/figure/F3/