Ikram ullah M.Phil Medical Lab Sciences

1. Human Papillomavirus, Measles, HIV and
Hepatitis Viruses
Presented By: Ikram Ullah
M.Phil MLSc
UoH

2. WHAT IS HPV
• HPV stands for human papillomavirus.There are lots of
different types of HPV.
• Genital HPV is a very common sexually transmitted
infection. No symptoms
• More than 100 types
– More than 60 cutaneous types
• Can lead to skin warts
– 40 mucosal types
• High risk – most common are HPV 16, 18, 31 and 45
causes 70% of cervical cancers
• Low risk- include HPV types 6, 11. causes 90% of ano-genital warts
•

3. How HPV looks like?
• Papillomaviruses are small, 52-55nm in
diameter.
• They are non-enveloped, icosahedral
particles.
• This shape is made up of 12 pentameric
and 60 hexameric capsomers
• Their carpsid is composed of two
proteins, a major (L1) and minor (L2).

4. HPV Transmission
• Direct skin-to-skin contact
– Usually, but not always sexual contact
• Infected birth canal
• Fomites (very rare)
• Reservoirs
• Infected human
• Mother to child through
Vaginal childbirth

6. Pathogenesis
• Virus infection initially occurs in the actively dividing basal cells
in the stratum germinativum
• Virus induced hyperplasia- results in increased cell division
• The cells subsequently undergo denaturation and
hyperkeratiniztion aggregating into nascent papilloma

7. Diagnosis & Treatment
• Can be detected in a
clinical exam;
– History
– Visual exam
– Pap smears
– DNA testing
• Can be treated by
removing the warts;
• The virus cannot be
removed, so the warts may
grow back.

8. Vaccine
 Two vaccines currently developed:
1. Gardasil – protects against HPV types 16, 18,
6 and 11.
2. Cervarix – protects against HPV types 16 and 18.
1

9. Measles
• Measles or Rubeola, is an acute viral illness. Single stranded,
negative sense enveloped RNA
• Caused by a virus in the family paramyxovirus
genus Morbillvurus
• The term Rubeola a Latin word was first used
to describe the disease in Middle Ages
• The incubation Period is approx. 10 days but varies from 7 to 18 days.
It is usually 14 days until the rash appears

10. Transmission
• Measles transmission is airborne by respiratory droplet nuclei spread
Or
• It can be transmitted by direct contact with infected nasal or throat
secretions

11. Sign & Symptoms
• Severe cough, conjunctivitis, coryza and Koplik’s spots on the
buccal mucosa. These are present for three to four days prior
to rash onset
• Generalised maculopapular rash, usually lasting three or more
days
• Fever (at least 38°C) present at the time of rash onset

12. Diagnosis
• Clinical diagnosis of measles requires a history of fever of at least
three days, with at least one of the three C's (cough, coryza,
conjunctivitis)
• Observation of Koplik's spots is also diagnostic of measles
• Alternatively, laboratory diagnosis of measles can be done with
confirmation of positive measles IgM antibodies or isolation of
measles virus RNA from respiratory specimens

13. • In patients where phlebotomy is not possible, saliva can be
collected for salivary measles-specific IgA testing
• The contact with any infected person in any way, including
semen through sex, saliva, or mucus, can cause infection

14. Prevention of Measles
• Isolation of cases from diagnosis until about 5-7 days after onset
of rash
• Disinfection of all articles soiled with secretion of nose and
throat
• Administration of measles immune globulin to susceptible
infants and children under 3 years of age

15. • Measles-mumps-rubella (MMR) vaccine at 9 to 12 months of
age and a second dose at four years of age
• The second dose is not a booster but is designed to vaccinate
the approximately 5% of children who do not seroconvert to
measles after the first dose of vaccine

16. Human Immunodeficiency Virus
• The human immunodeficiency virus is a lentivirus that causes
the acquired immunodeficiency syndrome (AIDS)
• Unlike some other viruses, the human body cannot get rid of
HIV. That means that once you have HIV, you have it for life
• Chimpanzee version of the immunodeficiency virus (called
simian immunodeficiency virus, or SIV) most likely was
transmitted to humans and mutated into HIV when humans
hunted these chimpanzees for meat and came into contact with
their infected blood
•

17. • Family: Retroviridae
• Subfamily:Orthoretrovirinae
• Genus:Lentivirus
• Species: HIV 1 / HIV2
 HIV 1- Isolated in America, Europe & central Africa
 HIV 2- In West Africa – Less virulent and not spread as widely and rapidly as
HIV 1

18. MORPHOLOGY
• It is roughly spherical - diameter of about 120 nm
• Composed of two copies of positive single stranded
RNA (Held together by protein P7) enclosed by a
conical capsid composed of viral protein P24
• The RNA genome consists of 9 genes - Three of these
genes: gag, pol, and env, contain information needed
to make the structural proteins for new virus particles.

19. • Inside of capsid are three enzymes required for HIV
replication: reverse transcriptase, integrase and protease
• A matrix composed of the viral protein P17 surrounds the
capsid ensuring the integrity of the virion particle
• The matrix is surrounded by phospholipids – 2 layers –
Embedded by (glycoprotein) – Spikes: 2 units – Gp41 and
Gp120

20. • HIV doesn't survive well outside the body
• May survive up to 7 days in dry blood
• Virus is inactivated under extreme changes of pH in
acidic and alkaline medium.

21. Transmission
• HIV is transmitted through blood, semen, vaginal fluid
and from infected mother to her child
 Sexual contact – HIV is predominantly a sexual
transmitted disease
 Contaminated needles
 Organ transplacentation
 Blood or blood products

22. Pathogenesis
• Receptor for virus is CD4 receptor. Therefore virus may
infect any cells having CD4 receptors on the surface
• The specific binding site to the virus is enveloped
glycoprotein (Gp120)
• Double stranded DNA integrated into genome of
infected cells causing latent infection
• From time to time lytic infection is initiated releasing
progeny virions which infect other cells.
• Long and variable incubation period of HIV infection is
because of the latency.

23. • Infected CD4 cells do not appear to release normal amount
of interleukins, interferon and other lymphokines.Therefore,
immune state of a person decreases
• Patients are unable to respond to new antigens.
• An important feature to HIV infection is the polyclonal
activation of B-lymphocytes.
• All classes of immunoglobulins are involved but level of
IgG and IgA particularly rose.
• In infants and children IgM is elevated. Hyper-γ-
globulinaemia is more of hindrance than help because it
is composed of mainly useless Ig

24. • Monocyte, macrophage function also affected. As a
result chemotaxis and antigen presentation and
intracellular killing by these cells are diminished.
• NK cells are also affected

25. SIGNS & SYMPTOMS
 Pneumonia, bronchitis, pleuritis, meningitis, dementia,
enteritis decrease body mass, diarrhea, carposious
sarcoma and other tumors etc.
• HIV infection has 4 stages
I. Incubation period (2-4weeks)
II. Stages of primary manifestation (years)
III. Stage of secondary manifestation
IV. Terminal stage (AIDS)

26. Laboratory Diagnosis
• Total count of leukocyte and lymphocyte (detect leucopenia), CD4
cells must be counted and the ratio between CD4 and CD8 cells is
detected, counting of platelets and rising level of IgG and IgA
• ELISA TEST, if positive the Westren blot is usually administered to confirm the
diagnosis
• Immuno assay for HIVp24 antigen
• PCR
• In order to prove presence of HIV, antibodies are detected:
1. HIV-1: antibodies to gp41, gp120, gp160, p24
2. HIV-2: antibodies to gp36, gp105, gp140

27. • HOME HIV TEST
• You swab fluid from your upper and lower gums and using a kit to test it
• Results are available within 20m minutes
• If positive you need to see to doctor to confirm the diagnosis
• If negative it needs to be to repeated in three months to confirm the result

28. Prevention
• Determination of people of risk group
• Identification of source of infection and control
• Health education – Sex should be practised by avoiding
exchange of body fluid, using sterile needles and syringes

29. Hepatitis A Virus
• Causes infectious hepatitis, Spread by fecal oral route,
results from the consumption of contaminated water, shellfish,
or other food
• It is a picornavirus, 27-nm, naked, icosahedral capsid, A
positive-sense single-stranded RNA, One serotype
• Like other picornaviruses, but HAV is not cytolytic and is
released by exocytosis
• Clinical isolates are difficult to grow in cell culture

30. Pathogenesis
• Although interferon limits viral replication, natural killer and
cytotoxic T cells are required to eliminate infected cells.
• Antibody, complement, and antibody-dependent cellular
cytotoxicity also facilitate clearance of the virus and
induction of immunopathology
• Icterus resulting from the damage of the liver occurs when
cell-mediated immune response and antibody to the virus
can be detected.

31. Transmission
• Spread rapidly because most infected people are
contagious 10 to 14 days before symptoms occur.
• HAV is released in stool in high concentrations and is
spread via fecal oral route.
• Spread in contaminated water, in food, and in dirty hands.
• Raw or improperly treated sewage can taint the water
supply and contaminate shellfish

32. Sign & Symptoms
• Immune-mediated damage to the liver
• Intensify for 4-6 days before the icteric (jaundice) phase.
• Can last up to 2 months.
• Initial symptoms: fever, fatigue, nausea, loss of appetite,
vomiting, and abdominal pain.

33. Diagnosis
• Most important: anti-HAV IgM
• Classical liver enzymes
• Virus isolation is not performed.
• Treatment, Prevention, Control:
• Interrupt the fecal-oral spread.
• Prophylaxis: immune serum globulin: before or early in incubation period
• Vaccine: Killed vaccine, recommended for all children < 1 years.

34. Hepatitis B Virus
• Previously known to cause serum hepatitis.
• Spread parenterally by blood or needles, by
sexual contact, and perinatally.
• Incubation period of 3 months.
• Might be followed by chronic hepatitis.
• Causally associated with primary hepatocellular carcinoma
(PHC).

35. • Major member of hepadnaviruses.
• Small enveloped DNA virus with several unusual
properties.
• Specifically, the genome is small, circular partly double
stranded of 3200 bases.

36. • The virion includes a protein kinase and a polymerase with
reverse transcriptase and ribonuclease H activity, as well
as a P protein attached to the genome.
• The virion is surrounded by an icosahedral capsid formed
by the hepatitis B core antigen (HBcAg) and an envelope
containing three forms of glycoprotein hepatitis B surface
antigen (HBsAg).
• HBsAg-containing particles are released into the serum

37. Pathogenesis
• HBV can cause acute or chronic, symptomatic or
asymptomatic disease determined by person’s immune
response.
• HBV found majorly in blood, but also in semen, saliva, milk,
vaginal and menstrual secretions, and amniotic fluid.
• The virus starts replication after 3 days of acquisition,
symptoms may not be observed for 45 days or longer
because they are primarily caused by immunopathology.

38. Acute infection
• Less symptomatic or asymptomatic in children.
• Long incubation
• fever, malaise, anorexia, nausea, vomiting, abdominal
discomfort, and chills, jaundice, dark urine, pale stool.

39. Chronic infection
• 5-10% of cases
• One third of those people have chronic active hepatitis
(continues destruction and causes scarring of the liver,
cirrhosis, liver failure, or PHC).
• The other two third have chronic passive hepatitis

40. Lab. Diagnosis
• The initial diagnosis can be made on basis of the clinical
symptoms and the presence of liver enzymes in blood.
• Serology describes the course and the nature of the
disease
• IgM anti-HBc is the best way to diagnose a recent acute
infection.
• The amount of virus is determined by quantitative genome
assays using PCR

41. Prevention
• Hepatitis B immune globulin may be administered within a
week of exposure.
• Chronic infection treatment: drugs targeted at the polymerase
or the nucleosides analogs for a year.
• Prevention: screening blood, safe sex, avoiding some lifestyles,
wearing gloves in hospitals....
• Vaccination: recommended for infants, children, and high risk
groups of people, a series of three injections

42. Hepatitis C Structure and Pathogenesis
• The only member of the Hepacivirus genus of the Falviviridae family.
• 6 genotypes. Positive sense RNA enveloped
• Viral RNA dependent RNA polymerase (gives antigen variability).
• The ability of HCV to remain cell associated and prevent host cell
death promotes persistent infection but results in liver disease later in
life
• It’s suggested that HCV may predispose the development of PHC.

43. Transmission and signs & symptoms
• HCV is transmitted primarily in the infected blood and sexually
• Almost every HIV infected people are HCV infected too
• The high incidence of chronic asymptomatic infections promotes the
spread.
• Acute Hepatitis ends with recovery.
• Severe rapid progression to cirrhosis.
• Chronic persistence often progresses to chronic active hepatitis.

44. Diagnosis and Prevention
• Laboratory diagnosis: based on ELISA recognition of anti-HCV
antibody or detection of the RNA genome
• Genome detection and quantitation by RT-PCR, branched-chain
DNA, and related techniques.
• Precautions for preventing HCV are similar for HBV

45. Hepatitis G Virus
• Resembles HCV in many ways.
• Flavivirus. Transmitted in blood, and has a predilection for
chronic hepatitis infection.
• It is identified by detection of the genome by RT-PCR or
other methods RNA detection

46. Hepatitis D Virus
• Single-stranded RNA, circular, forms a rod shape as a
result of its extensive base pairing.
• Uses HBV and targeted cell to replicate and produce its
protein.
• HBsAg is essential for packaging the virus.
• 40% of fulminant hepatitis infections

47. Hepatitis E Virus
• Spreads by fecal oral route. Especially in contaminated water.
• Calicivirus, RNA genome, naked capsid.
• More problematic in developing countries.
• Symptoms are similar to HAV , causes only acute disease.
• Infection is serious in pregnant women (mortality of 20%).

48. References
 A REVIEW ON: HIV/AIDS by Kapila, A. et al, 2016
 Hepatitis: A Review on Current and Future scenario by Pallavi k, et al. 2016
 California Association for Medical Lab. Technology by Les Revier
 Slideshares
 Wikipedia