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GENERAL VIROLOGY
Viruses
• Viruses are the smallest infectious
agents.
• They are obligatory intracellular
parasites because they have no
metabolic activity.
Viruses Can Infect All Organisms
In Nature
1. Bacteriophages: are bacterial viruses.
2. Plant viruses: include complete viruses
& viroids.
3. Animal viruses: infect insects or
vertebrates including man.
Differences between Viruses & Bacteria
• Viruses are very small in size, ranging form 20-
300 nm. So only seen by the electron
microscope (except poxviruses).
• Viruses contain only one type of nucleic acid
(DNA or RNA), never both.
• They are obligatory intracellular parasites, i.e.
can only replicate inside living cells.
• They can not be cultivated in the laboratory on
artificial culture media.
• They are not susceptible to antibacterial agents.
Viral Structure
Viral
Replication
PATHOGENESIS OF VIRAL DISEASES 1
I. Entry of viruses
• Viruses enter the body either by inhalation,
ingestion, contact (urogenital system) &
through skin (injections, blood transfusion,
insect & animal bites).
• Viruses usually replicate in the primary site
of entry. Some viruses produce disease at
the portal of entry (local infections), others
have to spread to distant organs (either via
the blood (viraemia), or by other means, e.g.
along nerves) & produce systemic or deep
viral infections.
Differences between Local &
Systemic Viral Infections
Systemic
Infections
Local
Infections
MeaslesRespiratory
(common cold
e.g. rhinovirus)
Specific disease
example
At distant sitesPortal of entrySite of pathology
Relatively longRelatively
short
Incubation period
PresentAbsentViraemia
Usually life-longUsually shortDuration of immunity
Usually not
important
importantRole of secretory IgA
II. Fate of Viral Infections
1.Inapparent or subclinical viral infections:
Viral infection without overt signs &
symptoms.
2. Apparent infections (disease): This may
be local or systemic with the appearance of
clinical signs & symptoms.
3. Persistent viral infections (chronic): the
virus is continuously detected with mild or
no clinical symptoms, e.g. chronic hepatitis
B.
II. Fate of viral infections
4. Latent viral infections: The virus persists
in a dormant form & may flare up
intermittently to produce disease, e.g.
herpes viruses.
5. Slow virus infections: Virus infections
with long incubation periods (months or
years), caused by:
- Conventional viruses, e.g. a variant of
measles virus which causes subacute
sclerosing panencephalitis (SSPE).
- Unconventional agents (prions).
LABORATORY DIAGNOSIS OF
VIRAL INFECTIONS
I. Direct detection of viruses
and/or their antigens.
II. Isolation of viruses.
III. Serological diagnosis.
IV. Skin tests.
I. Direct Detection of Viruses
1. Light microscopy.
2. Fluorescent microscopy.
3. Electron microscopy (EM).
4. IEM.
5. Immunoassays.
6. Molecular detection.
II. Isolation (Cultivation) of Viruses
• Viruses replicate only in living
susceptible cells.
• There are three main methods for
cultivation of viruses in the laboratory:
I. Cell culture (tissue culture).
II. Embryonated eggs.
III. Laboratory animals (intact animals).
Cell Culture
Embryonated
Egg
Lab. Animals
III. Serological Diagnosis
• It is an indirect method to detect antiviral
antibodies (e.g. ELISA).
• Usually 2 serum samples (paired serum) are
taken. The first in the acute phase and the
second 2-3 weeks later, to demonstrate a
rising titre (4 fold increase or more is
diagnostic).
• Only one sample may be used in the acute
stage to detect IgM.
IV. Skin Tests
Skin tests can be used as an indication of
CMI in some viral infections, e.g. mumps.
TREATMENT OF VIRAL INFECTIONS
• Viruses can not be treated with
antibiotics because they lack the
structural targets on which antibiotics
can act.
• Antiviral drugs include amantadine,
acyclovir, ribavirin, zidovudine &
interferons (IFNs).
Hepatitis Viruses
• Viruses infecting the liver as a primary
target:
– HAV: Picornaviridae (non-enveloped, positive-
sense ssRNA)
– HBV: Hepadnaviridae (enveloped, partially dsDNA)
– HCV: Flaviviridae (enveloped, +ssRNA)
– HDV: Deltaviridae (defective, ssRNA)
– HEV: Calicivirus (non-enveloped, +ssRNA)
– HGV: Flaviviridae (enveloped, +ssRNA)
• Viruses infecting the liver as a secondary
target: yellow fever virus, Epstein-Barr virus (EBV)
and cytomegalovirus (CMV).
HEPATITIS A VIRUS (HAV)
HEPATITIS A VIRUS (HAV)
• HAV causes hepatitis A (previously called infectious
hepatitis).
• The disease occurs in sporadic or epidemic forms.
• Transmission: Faeco-oral route.
• Incubation period: 2-6 weeks.
• C.P.: Fever, GIT symptoms (anorexia, nausea,
vomiting), jaundice.
• Usually mild symptoms, self-limited, no chronicity.
Laboratory Diagnosis
• Marked elevation of liver enzymes &
bilirubin.
• Detection of anti-HAV IgM (by ELISA or
RIA) during the acute phase.
• Detection of anti-HAV IgG during
convalescence.
• Detection of HAV particles in stools or
blood by E/M or PCR.
Prevention & Control
• Proper hand washing, chlorination or
boiling of drinking water.
• Proper sewage disposal.
• Inactivated vaccine (Havrix): 2 doses I.M.
at 0 & 6 months. Given to high-risk people
above 2 years in endemic countries.
• HAV-Ig for post-exposure prophylaxis to
prevent the disease in immunodeficient
persons.
HEPATITIS B VIRUS
(HBV)
HEPATITIS B VIRUS (HBV)
• HBV is a DNA virus of Hepadnaviridae family
that causes serum hepatitis.
• These are enveloped viruses & the intact virion,
known as the Dane particle, is spherical with 42 nm
diameter.
Modes of HBV Transmission
• Sexual contact (heterosexual or homosexual).
• Blood & blood products:
– Direct inoculation by needles (especially among
parenteral drug addicts).
– Other percutaneous exposures (including
tattooing, ear piercing, acupuncture, needle sticks
or other injuries from sharp instruments).
• Perinatally (mother to fetus): usually at the time
of delivery.
Risk Factors for Hepatitis B
• Sexual partner of a hepatitis patient or
carrier.
• Parenteral drug addicts.
• Infants of infected mothers.
• Household contacts with a hepatitis patient.
• Patients receiving transfusion of blood or
blood products e.g., haemophiliacs.
• Haemodialysis patients & staff.
• Occupational exposure to blood & infectious
body fluids (health care workers).
• Individuals undergoing tattooing.
Pathogenesis & Clinical
Presentations
• Incubation period: from 6 weeks - 6 months.
• Onset of the disease: gradual.
• Clinical manifestations:
– Perinatally infected infants generally have no clinical signs or
symptoms and infection produces typical illness in only 5-15%
of children aged 1-5 years.
– Older children and adults are symptomatic in 33-
50% of infections.
• Constitutional symptoms such as malaise and
anorexia may precede jaundice by 1-2 weeks.
Pathogenesis & Clinical
Presentations 2
• Clinical symptoms & signs: include nausea, vomiting,
abdominal pain and jaundice. Skin rashes, joint pains
and arthritis may occur. The liver is enlarged and tender.
• Most patients recover fully and spontaneously within 4-6
months.
• Chronic infection can lead to long term complications:
- Chronic active hepatitis & cirrhosis liver failure
& death.
- Hepatocellular carcinoma (HCC).
Laboratory Diagnosis
A. Hepatitis B virus Markers 1
(HBV Antigens & Antibodies)
1. HBsAg: can be detected in the blood during the
incubation period and active disease. It usually
declines within a period of 12 weeks. Its
persistence for more than 6 months indicates a
chronic carrier state.
2. Anti-HBs: appears late, with the disappearance
of HBsAg and denotes immunity.
3. HBcAg: is present only in the liver cells and can
not be detected in blood.
Laboratory Diagnosis
A. Hepatitis B virus Markers 2
4. Anti-HBc: of 2 Ig classes, IgM and IgG.
– IgM anti-HBc is detectable at the time of clinical onset
and declines within 6 months, thus it is a valuable
diagnostic test for recent HBV infection when other
markers are negative. (There is a period designated the
window phase during which HBsAg has disappeared
while anti-HBs is not yet detectable. During this phase,
IgM anti-HBc is always positive and diagnostic).
– IgG anti-HBc persists indefinitely as a marker of past
infection.
Laboratory Diagnosis
A. Hepatitis B virus Markers 3
5. HBeAg: It can be detected in the serum in the
late incubation period and during the acute
illness. Its presence is associated with high
infectivity of the patient. Its disappearance is a
good prognostic sign.
6. Anti-HBe: Its detection is a strong evidence of
recovery.
N.B.: Persistent HBeAg and absence of HBeAb is an
indication for treatment, as such a patient is developing
chronic active hepatitis.
Laboratory Diagnosis
B. DNA polymerase activity: demonstrated during
viraemic stage of HBV infection.
C. Viral DNA: can be detected by probe or PCR. It
is indicative of viral replication.
D. Liver function tests.
E. Liver biopsy: permits a tissue diagnosis of
hepatitis.
Prevention & Control
1. General Measures
• Screening of blood before transfusion.
• Use of disposable syringes, tattoo
needles … etc. Avoid recapping of the
used needles.
• Standard
precautions.
Prevention & Control
2. Specific Prophylaxis
Hepatitis B Vaccines
• Plasma-derived vaccines: containing
purified HBsAg obtained from serum of
HBsAg carriers ------ Unsafe.
Prevention & Control
2. Specific Prophylaxis
Recombinant
vaccines:
• by using HBsAg
synthesized by yeast.
• In 3 I.M. doses at 0, 1,
6 months.
• only in the deltoid
muscle of adults &
children or in the
anterolateral thigh of
neonates & infants.
Prevention & Control
Passive Immunization
Hepatitis B immunoglobulin (HBIG)
together with vaccination are given as
post-exposure prophylaxis to:
• Neonates born to HBsAg positive mothers.
• Those already exposed to HBV (e.g. HCW
after needle-prick injury).
HEPATITIS DELTA VIRUS (HDV)
• It is a unique defective virus, composed of a
core (ssRNA), surrounded by HBsAg.
• HDV can only replicate in patients with HBV
infection (either a co-infection or a super-
infection).
• As HDV is dependent on HBV it follows a
similar epidemiology. It can be controlled
through control of hepatitis B infection.
• Diagnosis: By PCR or detection of anti-HDV
antibodies.
HEPATITIS C VIRUS (HCV)
Epidemiology
• HCV has a worldwide distribution and is
particularly prevalent in the Middle East.
• Transmitted mainly parenterally through skin
and mucous membranes. Also there is
perinatal transmission (still 40% of cases
show no definable source or route of
infection).
• 50% of HCV infections are associated with
development of chronic active hepatitis that
ends in cirrhosis or HCC.
Laboratory Diagnosis
• Detection of anti-HCV antibodies by ELISA,
or the more specific RIBA test (recombinant
immunoblotting assay). Seroconversion may
take up to 6 months.
• PCR for detection of viral RNA in blood. This is
useful in:
– Diagnosis of early cases before seroconversion.
– Serologically confirmed cases to demonstrate
active viral replication and, thus, the need for
therapy.
– Follow up the response to treatment.
– Genotyping of HCV.
Control & Treatment
• Control: No specific vaccine is available.
Prevention is mainly directed at minimizing
exposure as that of preventing HBV infection.
• Treatment: A combination of alpha-interferon
and antiviral chemotherapy (ribavirin).
HEPATITIS E VIRUS (HEV)
• It is a Calicivirus (non-enveloped, +ssRNA),
characterized by faeco-oral transmission and a short
incubation period of about 6 weeks.
Diagnosis
• PCR is used to detect viral RNA in stools.
• Detection of anti-hepatitis E virus IgM & IgG by ELISA.
HEPATITIS G VIRUS
• HGV is a blood borne virus.
Diagnosis
• Anti-HGV antibodies in the serum can be
detected.
• Viral RNA can also be detected in blood by
PCR.
Thank You
RETROVIRUSES
Family Retroviridae
• The name is derived from the fact that
these viruses contain a reverse (retro)
transcriptase, i.e., RNA-dependent DNA
polymerase.
• This family contains HIV &HTLV.
Structure of HIV
Pathogenesis of HIV Infection 1
Cells that are infected by HIV
• CD4+ T helper lymphocytes: CD4 antigen is
the receptor for HIV.
• Monocytes/macrophages: They can act as a
reservoir of HIV.
• Follicular dendritic cells (FDCs): in lymph
nodes, which serve as a reservoir.
• Oligodendrocytes, astrocytes, neurones & glial
cells.
HIV Transmission
1. Sexual Transmission.
2. Blood & blood products (e.g. blood
transfusion, sharing syringes or accidental
needle prick injury).
3. Vertical Transmission: during pregnancy,
childbirth or through breast-feeding.
Disinfection
• 0.5% chlorine (hypochlorite) for
contaminated surfaces.
• 1% chlorine for rapid (10 min.)
disinfection of blood & body fluid spills and when
working with HIV cultures and virus preparations.
• Fresh 2% alkaline gluteraldehyde are effective,
provided that there is no organic matter.
• In contrast, 70% ethanol is ineffective unless
used with a prolonged contact time, up to 20 min.
Clinical Background
A. Acute HIV Infection
(Acute Retroviral Syndrome)
• During this phase, the blood contains many
viral particles that spread throughout the
body, seeding various organs, particularly the
lymphoid organs.
• After an incubation period of 2-4 weeks, up to
70% of HIV-infected individuals present as a
transient illness (acute retroviral syndrome),
characterized by acute flu-like or infectious
mononucleosis-like illness.
A. Acute HIV Infection
• Symptoms: fever, malaise, arthralgia,
myalgia, maculopapular rash, pharyngitis,
oral ulcers, lymphadenopathy, weight loss &
aseptic meningitis.
• Symptoms last between 7-10 days.
• It is an important differential diagnosis in
cases of fever of unknown origin,
maculopapular rash & lymphadenopathy.
B. Clinical Latency
• Acute HIV infection is followed by an
extended period of clinical latency with
no symptoms.
• Latency is due to:
– The rapid virus mutation.
– Depletion of cytotoxic T (Tc) cells.
– Loss of CD4+ T (Th) cell responses.
– The virus may hide within the chromosomes
of infected cells & away from recognition by
the immune system
C. AIDS
• The average AIDS incubation period is 8
- 10 years.
• HIV disease is characterized by a gradual
deterioration of immune function
(specially, the CD4+ T cells.
C. AIDS
• A healthy, uninfected person usually has
800 - 1,200 CD4+ T cells/mm3 of blood.
• During HIV infection, the number of
these cells progressively declines in the
blood.
• When CD4+ T cell count falls below
200/mm3, the infected person becomes
particularly vulnerable to the
opportunistic infections & cancers
characteristic of AIDS.
HIV Orofacial Manifestations
• Fungal infections:
– Oral candidiasis.
– Gingival erythema & angular cheilitis.
• Viral infections:
– Hairy leukoplakia.
– Kaposi sarcoma.
– Herpetic stomatitis.
– Papillomas.
• Bacterial infections: gingivitis & periodontitis.
• Cervical lymphadenopathy & lymphomas.
Diagnosis of HIV Infection
Diagnosis of HIV Infection
• Demonstration of virus (e.g. by PCR) or virus
components.
• Demonstration of immune response (HIV
antibody screening tests).
• CD4+ cell count: less than 200 cells/mm3.
Treatment
• No treatment is available that cures AIDS, but
a number of antiretroviral drugs have been
developed that suppress HIV replication,
thereby preventing the destruction of the
immune system.
• Drugs include:
RT inhibitors, protease inhibitors & fusion inhibitors.
Post-Exposure Chemoprophylaxis
• Needle stick injuries or puncture wounds, cuts, or
non-intact skin contaminated by spills or splashes
of specimens or blood and body fluids should be
thoroughly washed with soap and water and
non-irritating detergent. Bleeding from any
wound should be encouraged.
• In case of percutaneous penetration,
antiretroviral treatment should be started
immediately (a triple combination, which includes two
RT inhibitors & a protease inhibitor).
THANK YOU

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د حاتم البيطار استشاري وجراح الفم والاسنان 01005684344 اتصل للحجز بالعيادة محاضر طبي Dr.Hatem EL-Bitar

  • 2. Viruses • Viruses are the smallest infectious agents. • They are obligatory intracellular parasites because they have no metabolic activity.
  • 3. Viruses Can Infect All Organisms In Nature 1. Bacteriophages: are bacterial viruses. 2. Plant viruses: include complete viruses & viroids. 3. Animal viruses: infect insects or vertebrates including man.
  • 4.
  • 5. Differences between Viruses & Bacteria • Viruses are very small in size, ranging form 20- 300 nm. So only seen by the electron microscope (except poxviruses). • Viruses contain only one type of nucleic acid (DNA or RNA), never both. • They are obligatory intracellular parasites, i.e. can only replicate inside living cells. • They can not be cultivated in the laboratory on artificial culture media. • They are not susceptible to antibacterial agents.
  • 8. PATHOGENESIS OF VIRAL DISEASES 1 I. Entry of viruses • Viruses enter the body either by inhalation, ingestion, contact (urogenital system) & through skin (injections, blood transfusion, insect & animal bites). • Viruses usually replicate in the primary site of entry. Some viruses produce disease at the portal of entry (local infections), others have to spread to distant organs (either via the blood (viraemia), or by other means, e.g. along nerves) & produce systemic or deep viral infections.
  • 9. Differences between Local & Systemic Viral Infections Systemic Infections Local Infections MeaslesRespiratory (common cold e.g. rhinovirus) Specific disease example At distant sitesPortal of entrySite of pathology Relatively longRelatively short Incubation period PresentAbsentViraemia Usually life-longUsually shortDuration of immunity Usually not important importantRole of secretory IgA
  • 10. II. Fate of Viral Infections 1.Inapparent or subclinical viral infections: Viral infection without overt signs & symptoms. 2. Apparent infections (disease): This may be local or systemic with the appearance of clinical signs & symptoms. 3. Persistent viral infections (chronic): the virus is continuously detected with mild or no clinical symptoms, e.g. chronic hepatitis B.
  • 11. II. Fate of viral infections 4. Latent viral infections: The virus persists in a dormant form & may flare up intermittently to produce disease, e.g. herpes viruses. 5. Slow virus infections: Virus infections with long incubation periods (months or years), caused by: - Conventional viruses, e.g. a variant of measles virus which causes subacute sclerosing panencephalitis (SSPE). - Unconventional agents (prions).
  • 12. LABORATORY DIAGNOSIS OF VIRAL INFECTIONS I. Direct detection of viruses and/or their antigens. II. Isolation of viruses. III. Serological diagnosis. IV. Skin tests.
  • 13. I. Direct Detection of Viruses 1. Light microscopy. 2. Fluorescent microscopy. 3. Electron microscopy (EM). 4. IEM. 5. Immunoassays. 6. Molecular detection.
  • 14. II. Isolation (Cultivation) of Viruses • Viruses replicate only in living susceptible cells. • There are three main methods for cultivation of viruses in the laboratory: I. Cell culture (tissue culture). II. Embryonated eggs. III. Laboratory animals (intact animals).
  • 16. III. Serological Diagnosis • It is an indirect method to detect antiviral antibodies (e.g. ELISA). • Usually 2 serum samples (paired serum) are taken. The first in the acute phase and the second 2-3 weeks later, to demonstrate a rising titre (4 fold increase or more is diagnostic). • Only one sample may be used in the acute stage to detect IgM.
  • 17. IV. Skin Tests Skin tests can be used as an indication of CMI in some viral infections, e.g. mumps.
  • 18. TREATMENT OF VIRAL INFECTIONS • Viruses can not be treated with antibiotics because they lack the structural targets on which antibiotics can act. • Antiviral drugs include amantadine, acyclovir, ribavirin, zidovudine & interferons (IFNs).
  • 19.
  • 20.
  • 21. Hepatitis Viruses • Viruses infecting the liver as a primary target: – HAV: Picornaviridae (non-enveloped, positive- sense ssRNA) – HBV: Hepadnaviridae (enveloped, partially dsDNA) – HCV: Flaviviridae (enveloped, +ssRNA) – HDV: Deltaviridae (defective, ssRNA) – HEV: Calicivirus (non-enveloped, +ssRNA) – HGV: Flaviviridae (enveloped, +ssRNA) • Viruses infecting the liver as a secondary target: yellow fever virus, Epstein-Barr virus (EBV) and cytomegalovirus (CMV).
  • 22.
  • 24. HEPATITIS A VIRUS (HAV) • HAV causes hepatitis A (previously called infectious hepatitis). • The disease occurs in sporadic or epidemic forms. • Transmission: Faeco-oral route. • Incubation period: 2-6 weeks. • C.P.: Fever, GIT symptoms (anorexia, nausea, vomiting), jaundice. • Usually mild symptoms, self-limited, no chronicity.
  • 25. Laboratory Diagnosis • Marked elevation of liver enzymes & bilirubin. • Detection of anti-HAV IgM (by ELISA or RIA) during the acute phase. • Detection of anti-HAV IgG during convalescence. • Detection of HAV particles in stools or blood by E/M or PCR.
  • 26. Prevention & Control • Proper hand washing, chlorination or boiling of drinking water. • Proper sewage disposal. • Inactivated vaccine (Havrix): 2 doses I.M. at 0 & 6 months. Given to high-risk people above 2 years in endemic countries. • HAV-Ig for post-exposure prophylaxis to prevent the disease in immunodeficient persons.
  • 28. HEPATITIS B VIRUS (HBV) • HBV is a DNA virus of Hepadnaviridae family that causes serum hepatitis. • These are enveloped viruses & the intact virion, known as the Dane particle, is spherical with 42 nm diameter.
  • 29. Modes of HBV Transmission • Sexual contact (heterosexual or homosexual). • Blood & blood products: – Direct inoculation by needles (especially among parenteral drug addicts). – Other percutaneous exposures (including tattooing, ear piercing, acupuncture, needle sticks or other injuries from sharp instruments). • Perinatally (mother to fetus): usually at the time of delivery.
  • 30. Risk Factors for Hepatitis B • Sexual partner of a hepatitis patient or carrier. • Parenteral drug addicts. • Infants of infected mothers. • Household contacts with a hepatitis patient. • Patients receiving transfusion of blood or blood products e.g., haemophiliacs. • Haemodialysis patients & staff. • Occupational exposure to blood & infectious body fluids (health care workers). • Individuals undergoing tattooing.
  • 31. Pathogenesis & Clinical Presentations • Incubation period: from 6 weeks - 6 months. • Onset of the disease: gradual. • Clinical manifestations: – Perinatally infected infants generally have no clinical signs or symptoms and infection produces typical illness in only 5-15% of children aged 1-5 years. – Older children and adults are symptomatic in 33- 50% of infections. • Constitutional symptoms such as malaise and anorexia may precede jaundice by 1-2 weeks.
  • 32. Pathogenesis & Clinical Presentations 2 • Clinical symptoms & signs: include nausea, vomiting, abdominal pain and jaundice. Skin rashes, joint pains and arthritis may occur. The liver is enlarged and tender. • Most patients recover fully and spontaneously within 4-6 months. • Chronic infection can lead to long term complications: - Chronic active hepatitis & cirrhosis liver failure & death. - Hepatocellular carcinoma (HCC).
  • 33. Laboratory Diagnosis A. Hepatitis B virus Markers 1 (HBV Antigens & Antibodies) 1. HBsAg: can be detected in the blood during the incubation period and active disease. It usually declines within a period of 12 weeks. Its persistence for more than 6 months indicates a chronic carrier state. 2. Anti-HBs: appears late, with the disappearance of HBsAg and denotes immunity. 3. HBcAg: is present only in the liver cells and can not be detected in blood.
  • 34. Laboratory Diagnosis A. Hepatitis B virus Markers 2 4. Anti-HBc: of 2 Ig classes, IgM and IgG. – IgM anti-HBc is detectable at the time of clinical onset and declines within 6 months, thus it is a valuable diagnostic test for recent HBV infection when other markers are negative. (There is a period designated the window phase during which HBsAg has disappeared while anti-HBs is not yet detectable. During this phase, IgM anti-HBc is always positive and diagnostic). – IgG anti-HBc persists indefinitely as a marker of past infection.
  • 35. Laboratory Diagnosis A. Hepatitis B virus Markers 3 5. HBeAg: It can be detected in the serum in the late incubation period and during the acute illness. Its presence is associated with high infectivity of the patient. Its disappearance is a good prognostic sign. 6. Anti-HBe: Its detection is a strong evidence of recovery. N.B.: Persistent HBeAg and absence of HBeAb is an indication for treatment, as such a patient is developing chronic active hepatitis.
  • 36. Laboratory Diagnosis B. DNA polymerase activity: demonstrated during viraemic stage of HBV infection. C. Viral DNA: can be detected by probe or PCR. It is indicative of viral replication. D. Liver function tests. E. Liver biopsy: permits a tissue diagnosis of hepatitis.
  • 37. Prevention & Control 1. General Measures • Screening of blood before transfusion. • Use of disposable syringes, tattoo needles … etc. Avoid recapping of the used needles. • Standard precautions.
  • 38. Prevention & Control 2. Specific Prophylaxis Hepatitis B Vaccines • Plasma-derived vaccines: containing purified HBsAg obtained from serum of HBsAg carriers ------ Unsafe.
  • 39. Prevention & Control 2. Specific Prophylaxis Recombinant vaccines: • by using HBsAg synthesized by yeast. • In 3 I.M. doses at 0, 1, 6 months. • only in the deltoid muscle of adults & children or in the anterolateral thigh of neonates & infants.
  • 40. Prevention & Control Passive Immunization Hepatitis B immunoglobulin (HBIG) together with vaccination are given as post-exposure prophylaxis to: • Neonates born to HBsAg positive mothers. • Those already exposed to HBV (e.g. HCW after needle-prick injury).
  • 41.
  • 42. HEPATITIS DELTA VIRUS (HDV) • It is a unique defective virus, composed of a core (ssRNA), surrounded by HBsAg. • HDV can only replicate in patients with HBV infection (either a co-infection or a super- infection). • As HDV is dependent on HBV it follows a similar epidemiology. It can be controlled through control of hepatitis B infection. • Diagnosis: By PCR or detection of anti-HDV antibodies.
  • 44. Epidemiology • HCV has a worldwide distribution and is particularly prevalent in the Middle East. • Transmitted mainly parenterally through skin and mucous membranes. Also there is perinatal transmission (still 40% of cases show no definable source or route of infection). • 50% of HCV infections are associated with development of chronic active hepatitis that ends in cirrhosis or HCC.
  • 45. Laboratory Diagnosis • Detection of anti-HCV antibodies by ELISA, or the more specific RIBA test (recombinant immunoblotting assay). Seroconversion may take up to 6 months. • PCR for detection of viral RNA in blood. This is useful in: – Diagnosis of early cases before seroconversion. – Serologically confirmed cases to demonstrate active viral replication and, thus, the need for therapy. – Follow up the response to treatment. – Genotyping of HCV.
  • 46. Control & Treatment • Control: No specific vaccine is available. Prevention is mainly directed at minimizing exposure as that of preventing HBV infection. • Treatment: A combination of alpha-interferon and antiviral chemotherapy (ribavirin).
  • 47. HEPATITIS E VIRUS (HEV) • It is a Calicivirus (non-enveloped, +ssRNA), characterized by faeco-oral transmission and a short incubation period of about 6 weeks. Diagnosis • PCR is used to detect viral RNA in stools. • Detection of anti-hepatitis E virus IgM & IgG by ELISA.
  • 48. HEPATITIS G VIRUS • HGV is a blood borne virus. Diagnosis • Anti-HGV antibodies in the serum can be detected. • Viral RNA can also be detected in blood by PCR.
  • 51. Family Retroviridae • The name is derived from the fact that these viruses contain a reverse (retro) transcriptase, i.e., RNA-dependent DNA polymerase. • This family contains HIV &HTLV.
  • 53. Pathogenesis of HIV Infection 1 Cells that are infected by HIV • CD4+ T helper lymphocytes: CD4 antigen is the receptor for HIV. • Monocytes/macrophages: They can act as a reservoir of HIV. • Follicular dendritic cells (FDCs): in lymph nodes, which serve as a reservoir. • Oligodendrocytes, astrocytes, neurones & glial cells.
  • 54. HIV Transmission 1. Sexual Transmission. 2. Blood & blood products (e.g. blood transfusion, sharing syringes or accidental needle prick injury). 3. Vertical Transmission: during pregnancy, childbirth or through breast-feeding.
  • 55. Disinfection • 0.5% chlorine (hypochlorite) for contaminated surfaces. • 1% chlorine for rapid (10 min.) disinfection of blood & body fluid spills and when working with HIV cultures and virus preparations. • Fresh 2% alkaline gluteraldehyde are effective, provided that there is no organic matter. • In contrast, 70% ethanol is ineffective unless used with a prolonged contact time, up to 20 min.
  • 56. Clinical Background A. Acute HIV Infection (Acute Retroviral Syndrome) • During this phase, the blood contains many viral particles that spread throughout the body, seeding various organs, particularly the lymphoid organs. • After an incubation period of 2-4 weeks, up to 70% of HIV-infected individuals present as a transient illness (acute retroviral syndrome), characterized by acute flu-like or infectious mononucleosis-like illness.
  • 57. A. Acute HIV Infection • Symptoms: fever, malaise, arthralgia, myalgia, maculopapular rash, pharyngitis, oral ulcers, lymphadenopathy, weight loss & aseptic meningitis. • Symptoms last between 7-10 days. • It is an important differential diagnosis in cases of fever of unknown origin, maculopapular rash & lymphadenopathy.
  • 58. B. Clinical Latency • Acute HIV infection is followed by an extended period of clinical latency with no symptoms. • Latency is due to: – The rapid virus mutation. – Depletion of cytotoxic T (Tc) cells. – Loss of CD4+ T (Th) cell responses. – The virus may hide within the chromosomes of infected cells & away from recognition by the immune system
  • 59. C. AIDS • The average AIDS incubation period is 8 - 10 years. • HIV disease is characterized by a gradual deterioration of immune function (specially, the CD4+ T cells.
  • 60. C. AIDS • A healthy, uninfected person usually has 800 - 1,200 CD4+ T cells/mm3 of blood. • During HIV infection, the number of these cells progressively declines in the blood. • When CD4+ T cell count falls below 200/mm3, the infected person becomes particularly vulnerable to the opportunistic infections & cancers characteristic of AIDS.
  • 61. HIV Orofacial Manifestations • Fungal infections: – Oral candidiasis. – Gingival erythema & angular cheilitis. • Viral infections: – Hairy leukoplakia. – Kaposi sarcoma. – Herpetic stomatitis. – Papillomas. • Bacterial infections: gingivitis & periodontitis. • Cervical lymphadenopathy & lymphomas.
  • 62. Diagnosis of HIV Infection
  • 63.
  • 64. Diagnosis of HIV Infection • Demonstration of virus (e.g. by PCR) or virus components. • Demonstration of immune response (HIV antibody screening tests). • CD4+ cell count: less than 200 cells/mm3.
  • 65. Treatment • No treatment is available that cures AIDS, but a number of antiretroviral drugs have been developed that suppress HIV replication, thereby preventing the destruction of the immune system. • Drugs include: RT inhibitors, protease inhibitors & fusion inhibitors.
  • 66. Post-Exposure Chemoprophylaxis • Needle stick injuries or puncture wounds, cuts, or non-intact skin contaminated by spills or splashes of specimens or blood and body fluids should be thoroughly washed with soap and water and non-irritating detergent. Bleeding from any wound should be encouraged. • In case of percutaneous penetration, antiretroviral treatment should be started immediately (a triple combination, which includes two RT inhibitors & a protease inhibitor).