Human immunodeficiency virus infection and

Acquired immune deficiency syndrome

(HIV/AIDS) is a spectrum of conditions caused
by infection with the Human
immunodeficiency virus (HIV).
 As the infection progresses, it interferes
more and more with the immune system,
making the person much more susceptible
to common infections, like tuberculosis, as
well as opportunistic infections and tumors
that do not usually affect people who have
working immune systems. The late
symptoms of the infection are referred to as
AIDS.
 By September 1982 , two separate research
groups leg by Robert Gallo / USA/ and Luc
Montagnier /France/ declared that a new
Retrovirus may have been infecting AIDS
patients.
 Genetic research indicates that HIV

originated in west-central Africa during the

early 20th century. AIDS was first
recognized by the United States Centers for
Disease Control and Prevention (CDC) in
1981.
 Serologic testing was started in 1985.
 Anti-retroviral therapy was first
started in 1986.
 Combination anti-retroviral therapy
(Highly Active Antiretroviral Therapy
– HAART) in 1996.
 Etiology
 HIV is a member of the genus Lentivirus,
part of the family Retroviridae.
Lentiviruses share many morphological and
biological characteristics.
 Two types of HIV have been characterized:
HIV-1 and HIV-2. HIV-1 is the virus that
was originally discovered. It is more
virulent, more infective, and is the cause of
the majority of HIV infections globally.
 HIV 1
 Most common in sub-Saharan Africa and
throughout the world
 Groups M, N, and O

 Pandemic dominated by Group M

 HIV 2
 Most often found in West Central Africa,
parts of Europe and Asia
  Lentiviruses are transmitted as single-
stranded, positive-sense, enveloped RNA
viruses. Upon entry into the target cell, the
viral RNA genome is converted (reverse
transcribed) into double-stranded DNA by a
virally encoded reverse transcriptase that is
transported along with the viral genome in the
virus particle. The resulting viral DNA is then
imported into the cell nucleus and integrated
into the cellular DNA by a virally encoded
integrase and host co-factors.
  HIV can also disseminate by direct
transmission from one cell to another by a
process of cell-to-cell spread.
 Both HIV-1 and HIV-2 are believed to have
originated in non-human primates in West-
Central Africa and were transferred to
human in the early 20th century.
 HIV is different in structure from other
Retroviruses. It is composed of 2 copies of
positive single- stranded RNA that code for
the virus,s nine genes enclosed by a conical
capsid composed of 2000 copies of the viral
protein p24. The single- stranded RNA is
tightly bound to nucleocapsid proteins p7,
and enzymes needed for the development of
the virion such as reverse transcriptase,
protease and integrase.
 History
 The initial cases were a cluster of injecting
drug users and homosexual men with no
known cause of impaired immunity who
showed symptoms of Pneumocystis jiruvecii
pneumonia, a rare opportunistic infection
that was known to occur in people with very
compromised immune systems. Soon
thereafter, an unexpected number of
homosexual men developed a previously
rare skin cancer called Kaposi's sarcoma.
 Transmission
 Routes of transmission:
 Sexual transmission.

 Exposure to infected blood or blood products.

 Use of contaminated clotting factors by

hemophilians.
 Sharing contaminated needles ( drug users).

 Transplantation of infected tissues or organs.

 Mother to fetus, perinatal transmission

variable, dependent on viral load and mother’s

CD 4 count.
 Sexual transmission

- Sexually active group

- Man who have sex with man /MSM/
- Multiple sex partners
Exposure to blood-borne pathogens

This transmission route is particulary

relevant to intravenous drug users,
haemophilians and recipients of blood
transfusions and blood products.
 Parental transmission

The transmission of the virus from the

mother to the child can occur in utero
during the last weeks of pregnancy and
at childbirth. In the absence of
treatment the transmission rate
between a mother and her child during
pregnancy, labor and delivery is 25%.
HIV/ AIDS is a global pandemic. As of
approximately 38 million people have
HIV worldwide – 10 million are less
than 25 years old.
 Pathophysiology

The pathophysiology of AIDS is complex,

as is the case with all syndromes.
Ultimately, HIV causes AIDS by
depleting CD4 ( T-helpers) lymphocites.
This weakens the immune system and
allows opportunistic infections.
 Cells affects
 HIV attaches to susceptible host cell.
 Site of attachment is the CD4 antigen

found on a variety of cells

 T helper cells

 macrophages

 monocytes

microglial brain cells

Central nervous system:
- Microglia of the nervous system

- Astrocytes

- Oligodendrocytes

- Neurones- indirectly by the action of

citokines and the gp120.

 Early Phase of HIV Infection

In early phase HIV infection, initial

viruses are M-tropic. Their envelope
glycoprotein 120 is able to bind to CD4
molecules and chemokine receptors
called CCR5 found on macrophages.
1.Interaction between viral envelope proteins
and CD4 receptor and co-receptors leads to
binding of the viral envelope and host
cytoplasmic membrane
2.Viral reverse transcriptase catalyses the
conversion of viral RNA into DNA
3.Proviral DNA enters the nucleus and
becomes integrated into chromosomal DNA of
host cell (catalyzed by integrase)
4. Expression of viral genes leads to
production of viral RNA and proteins.
5. Protease enzyme cleaves proteins into
functional mature products.
6. Viral proteins and viral RNA are
assembled at the cell surface into the new
viral particles and leave the host through
budding.
 After a period of latency lasting up to 10
years viral replication is triggered and
occurs at high rate.
 CD4 cell may be destroyed in the process,
body attempts to replace lost CD4 cells, but
over the course of many years body is
unable to keep the count at a safe level.
 Destruction of large numbers of CD4 cause
symptoms of HIV to appear with increased
susceptibility to opportunistic infections
diseases and malignancy.
 Primary HIV Syndrome

Cold or flu-like symptoms may occur 6 to 12 weeks

after infection:
 lymphadenopathy

 fever

 rash

 headache

 fatigue

 diarrhea

 sore throat

 neurologic manifestation
 Clinical Latency Period
 HIV continues to reproduce, CD4 count
gradually declines from its normal value of 500-
1200.
 Once CD4 count drops below 500, HIV infected
person at risk for opportunistic infections.
 The following diseases are predictive of the
progression to AIDS:
 persistent herpes-zoster infection

 oral candidiasis (thrush)

 oral hairy leukoplakia

 Kaposi’s sarcoma (KS)

 AIDS
 If preventative medications not started the HIV
infected person is now at risk for:

 Pneumocystis jiruvecii pneumonia

 Cryptococcal meningitis
 Toxoplasmosis

 Mycobacterium tuberculosis
 Cytomegalovirus infection
 Lymphoma
 Dementia
 Most deaths occur with CD4 counts below 50.
 Treatment

HAART therapy ( Highly Affective Anti-

Retroviral Therapy)
Anti-Retroviral therapy is recommended
if patient is asymptomatic or
symptomatic stage.
The three main transmission routes of
HIV are sexual contact, exposure to
infected bogy fluids or tissues, and
from mother to fetus or child during
perinatal period. It is possible to find
HIV in the salvia, tears, milk, urine of
infected individuals, but infection by
these secretions, and the risk of
infection is negligible.
 Methods of control
A. Preventive measures:
 HIV/AIDS prevention programs can be

effective only with full community and

political commitment to change and/or
reduce high HIV-risk behaviours.
 Public and school health education
must stress that having multiple and
especially concurrent and/or
overlapping sexual partners or sharing
drug paraphernalia both increase the
risk of HIV infection.
 HIV testing and counselling is an
important intervention for raising
awareness of HIV status, promoting
behavioural change and diagnosing
HIV infection. HIV testing and
counselling can be undertaken for:
 a) persons who are ill or involved in
high-risk behaviours,
 b) attenders at antenatal clinics, to
diagnose maternal infection and
prevent vertical transmission
 c) couple counselling (marital or
premarital)
 d) anonymous and/or confidential
HIV counselling and testing for the
“worried well”
 All pregnant women must be counselled
about HIV early in pregnancy and
encouraged to undertake an HIV test as a
routine part of standard antenatal care.

 Those found to be HIV-positive take a

course of AR treatment, to reduce the risk
of their infant being infected.
 Care must be taken in handling, using and
disposing of needles or other sharp
instruments.

 Health care workers should wear latex

gloves, eye protection and other personal
protective equipment in order to avoid
contact with blood or with fluids.
 WHO recommends immunization of
asymptomatic HIV infected children with
the vaccines; those who are symptomatic
should not receive BCG vaccine.

 Live Measles-Mumps-Rubella and Polio

vaccines are recommended for all HIV-
infected children.
 Control of patient, contacts and the
immediate environment
 1) Report to local health authority: Official
reporting of AIDS cases is obligatory in most
countries.
 Official reporting of HIV infections is required in

some areas
 2) Isolation: Isolation of the HIV-positive person is

unnecessary and ineffective.

Universal precautions apply to all hospitalized
patients.
 3) Concurrent disinfection: Of equipment
contaminated with blood or body fluids and with
excretions and secretions visibly contaminated
with blood and body fluids
 4) Quarantine: Not applicable.

 5) Immunization of contacts: Not applicable.

 6) Notification of contacts and source of infection:

The infected patient should ensure notification of
sexual partners whenever possible.
 All donated units of blood must be tested
for HIV antibody; only donations testing
negative can be used.

 People who have engaged in behaviours that

place them at increased risk of HIV
infection should not donate plasma, blood,
organs for transplantation, tissue or cells.

 Only clotting factor products that have been

screened and treated to inactivate HIV must
be used.
 HIV Disease- Summary
 HIV multiples inside the CD4 cells, destroying
them
 As CD4 cell count decreases and viral load
( number of copies of HIV in the blood)
increases, the immune defenses are weakened
 HIV-infected people become vulnerable to
opportunistic infections
 Without AR treatment, HIV progresses to
symptomatic disease and AIDS
 Key Points
 HIV is a global pandemic and the
number of people living with HIV
continues to increase worldwide
 HIV epidemic is especially severe in
resource- constrained settings
 HIV is a virus that destroys the
immune system, leading to
opportunistic infections
 The progression from initial infection with
HIV to end-stage AIDS varies from person
to person and can take more than 10 years
 HIV-positive women who are pregnant are
at risk of passing HIV infection to their
newborn.
 Viral Hepatitis type B
 Hepatitis B is a viral infection that attacks
the liver and can cause both acute and
chronic disease.
 The virus is transmitted through contact
with the blood or other body fluids of an
infected person.
 An estimated 350 million people are
chronically infected with hepatitis B
(defined as hepatitis B surface antigen
positive for at least 6 months).
 More than 780 000 people die every year
due to complications of hepatitis B,
including cirrhosis and liver cancer.
 Hepatitis B is an important occupational
hazard for health workers.
 However, it can be prevented by currently
available safe and effective vaccine.
 Geographical distribution

 Hepatitis B prevalence is highest in sub-Saharan

Africa and East Asia, where between 5–10% of the
adult population is chronically infected. High rates
of chronic infections are also found in the
southern parts of Eastern and Central Europe. In
the Middle East and the Indian subcontinent, an
estimated 2–5% of the general population is
chronically infected. Less than 1% of the
population in Western Europe and North America
is chronically infected.
 Etiology
 Hepatitis B is an infection of the liver caused by the
Hepatitis B virus /HBV/. HBV is a double- stranded
DNA virus, member of the Hepadnavirus family.
 HBsAg – stimulates protective antibodies, a marker
for current infection
 HBcAg – localized within liver cells, identifies acute
infection, anti-HBcAg persists for life and is a
marker of past infection
 HBeAg – a marker of active replication and
infectivity
 The HBV is 50 to 100 times more infectious
than HIV.
The virus is divided into four major serotypes
/ adr, adw, ayr, ayw/ based on antigenic
epitopes presented on its envelope proteins,
and into eight genotypes / A-H/. The
genotypes have a distinct geographical
distribution and are used in tracing the
evolution and transmission of the virus.
Genotype A is most commonly found in the
Americas, Africa, India and Western
Europe. Genotype B is most commonly
found in Asia and USA. Genotype C is most
common in Japan, Korea and China, South-
East Asia.
 Pathogenesis

HBV primarily interferes with the functions

of the liver by replicating in hepatocytes.
Cytotoxic T-lymphocytes /CTLs/ eliminate
HBV infection by killing infected cells and
producing antiviral cytokines.
 Transmission
 The hepatitis B virus can survive outside the
body for at least 7 days. During this time,
the virus can still cause infection if it enters
the body of a person who is not protected by
the vaccine. The incubation period of the
hepatitis B virus is 75 days on average, but
can vary from 6 weeks to 6 months. The
virus may be detected within 30 to 60 days
after infection and can persist and develop
into chronic hepatitis B.
 In highly endemic areas, hepatitis B is most
commonly spread from mother to child at
birth (perinatal transmission), or through
horizontal transmission (exposure to
infected blood), especially from an infected
child to an uninfected child during the first 5
years of life. The development of chronic
infection is very common in infants infected
from their mothers or before the age of 5
years.
 Hepatitis B is also spread by percutaneous
or mucosal exposure to infected blood and
various body fluids, as well as through
saliva, menstrual, vaginal, and seminal
fluids. Sexual transmission of hepatitis B
may occur, particularly in unvaccinated
men who have sex with men and
heterosexual persons with multiple sex
partners or contact with sex workers.
 In addition, infection can occur during
medical, surgical and dental procedures,
tattooing, or through the use of razors and
similar objects that are contaminated with
infected blood.
 Signs and symptoms
Most people do not experience any symptoms
during the acute infection phase. However,
some people have acute illness with symptoms
that last several weeks, including yellowing of
the skin and eyes (jaundice), dark urine,
extreme fatigue, nausea, vomiting and
abdominal pain.
 A small subset of persons with acute
hepatitis can develop acute liver failure
which can lead to death.
 In some people, the hepatitis B virus can
also cause a chronic liver infection that can
later develop into cirrhosis of the liver or
liver cancer.
Chronic infection with HBV either may be
asymptomatic or may be associated with a
chronic inflammation of the liver /chronic
hepatitis/ , leading to cirrhosis over a period
of several years. This type of infection
dramatically increases the incidence of
hepatocellular carcinoma /liver cancer/ .
 Diagnosis
 Acute HBV infection is characterized by the
presence of HBsAg and immunoglobulin M
(IgM) antibody to the core antigen. During
the initial phase of infection, patients are
also seropositive for HBeAg. HBeAg is
usually a marker of high levels of
replication of the virus. The presence of
HBeAg indicates that the blood and body
fluids of the infected individual are highly
contagious.
Chronic infection is characterized by the
persistence of HBsAg for at least 6 months
(with or without concurrent HBeAg).
Persistence of HBsAg is the principal
marker of risk for developing chronic liver
disease and liver cancer (hepatocellular
carcinoma) later in life.
 Prevention
 The hepatitis B vaccine is the mainstay of
hepatitis B prevention. WHO recommends
that all infants receive the hepatitis B vaccine
as soon as possible after birth, preferably
within 24 hours. The birth dose should be
followed by 3 doses to complete the primary
series.
 4 doses schedule of Hepatitis B vaccine, with
the first dose (monovalent- Engerix B) being
given at birth and combined vaccine
Hexacim given at 2, 3 and 4 months.
Hexacim is a vaccine against Diphtheria,
Tetanus, Pertussis, Poliomielitis,
Haemophilus influenzae type B and Viral
Hepatitis B.
All children and adolescents younger than
18 years-old and not previously vaccinated
should receive the vaccine if they live in
countries where there is low or intermediate
endemicity. In those settings it is possible
that more people in high-risk groups may
acquire the infection and they should also
be vaccinated. They include:
 people who frequently require blood or
blood products, dialysis patients, recipients
of solid organ transplantations;
 people interned in prisons;
 persons who inject drugs;
 household and sexual contacts of people
with chronic HBV infection;
 people with multiple sexual partners;
 health-care workers and others who may be
exposed to blood and blood products
through their work;
 travellers who have not completed their
hepatitis B vaccination series, who should
be offered the vaccine before leaving for
endemic areas.
 The vaccine has an excellent record of
safety and effectiveness. Since 1982, over 1
billion doses of hepatitis B vaccine have
been used worldwide. In many countries
where 8–15% of children used to become
chronically infected with the hepatitis B
virus, vaccination has reduced the rate of
chronic infection to less than 1% among
immunized children.
  In addition, implementing of blood safety
strategies, including quality-assured screening of
all donated blood and blood components used for
transfusion, can prevent transmission of HBV.
Safe injection practices, eliminating unnecessary
and unsafe injections, can be effective strategies to
protect against HBV transmission. Further more,
safer sex practices, including minimizing the
number of partners and using barrier protective
measures (condoms), also protect against
transmission.
 Viral Hepatitis type C
 Hepatitis C is a liver disease caused by the hepatitis
C virus: the virus can cause both acute and chronic
hepatitis infection, ranging in severity from a mild
illness lasting a few weeks to a serious, lifelong
illness.
 The hepatitis C virus is a bloodborne virus and the
most common modes of infection are through
unsafe injection practices; inadequate sterilization
of medical equipment; and the transfusion of
unscreened blood and blood products.
 150 million people globally have chronic hepatitis C
infection.
 A significant number of those who are chronically
infected will develop liver cirrhosis or liver cancer.
 Approximately 200 000 people die each year from
hepatitis C-related liver diseases.
 Antiviral medicines can cure approximately 90%
of persons with hepatitis C infection, there by
reducing the risk of death from liver cancer and
cirrhosis, but access to diagnosis and treatment is
low.
 There is currently no vaccine for hepatitis C;
however research in this area is ongoing.
 Hepatitis C virus (HCV) causes both acute
and chronic infection. Acute HCV infection
is usually asymptomatic, and is only very
rarely associated with life-threatening
disease. About 15–25% of infected persons
spontaneously clear the virus within 6
months of infection without any treatment.
 The remaining 85% of persons will develop
chronic HCV infection. Of those with
chronic HCV infection, the risk of cirrhosis
of the liver is 30% within 20 years.
 Geographical distribution

Hepatitis C is found worldwide. The most

affected regions are Africa and Central and
East Asia. Depending on the country,
hepatitis C infection can be concentrated in
certain populations (for example, among
people who inject drugs); and/or in general
populations. There are multiple strains (or
genotypes) of the HCV virus and their
distribution varies by region.
 Transmission
The hepatitis C virus is a bloodborne virus. It is most
commonly transmitted through:
injecting drug use through the sharing of injection

equipment;
in health care settings due to inadequate sterilization

of medical equipment, especially syringes and needles;

the transfusion of unscreened blood and blood

products;
HCV can also be transmitted sexually and can be

passed from an infected mother to her baby; however

these modes of transmission are much less common.
 Symptoms
 The incubation period for hepatitis C is 2-6
weeks. Following initial infection,
approximately 80% of people do not exhibit
any symptoms. Those who are acutely
symptomatic may exhibit fever, fatigue,
decreased appetite, nausea, vomiting,
abdominal pain, dark urine, grey-coloured
faeces, joint pain and jaundice (yellowing of
skin and the eyes).
 Screening and diagnosis

 Due to the fact that acute HCV infection is

usually asymptomatic, few people are
diagnosed during the acute phase. In those
people who go on to develop chronic HCV
infection, the infection is also often
undiagnosed because the infection remains
asymptomatic until decades after infection
when symptoms develop secondary to
serious liver damage.
 HCV infection is diagnosed in 2 steps:
 Screening for anti-HCV antibodies with a
serological test identifies people who have been
infected with the virus.
 If the test is positive for anti-HCV antibodies, a
nucleic acid test for HCV RNA is needed to
confirm chronic HCV infection because about 15–
25% of people infected with HCV spontaneously
clear the infection by a strong immune response
without the need for treatment.
Populations at increased risk of HCV
infection include:
 people who inject drugs
 recipients of infected blood products or invasive
procedures in health-care facilities with inadequate
infection control practices
 children born to mothers infected with HCV
 people with sexual partners who are HCV-infected
 people with HIV infection
 prisoners or previously incarcerated person
people who have had tattoos or piercings.
 Prevention

 Primary prevention
 There is no vaccine for hepatitis C,

therefore prevention of HCV infection

depends upon reducing the risk of exposure
to the virus in health-care settings, in higher
risk populations, for example, people who
inject drugs, and through sexual contact.
 The following list provides a limited example of
primary prevention interventions recommended by
WHO:
 hand hygiene: including surgical hand preparation,

hand washing and use of gloves;

 safe handling and disposal of sharps and waste;

 provision of comprehensive harm-reduction services

to people who inject drugs including sterile injecting

equipment;
 testing of donated blood for hepatitis B and C (as

well as HIV and syphilis);

 training of health personnel;

 promotion of correct and consistent use of condoms.

 Secondary prevention
 For people infected with the hepatitis C virus, WHO
recommends:
 education and counselling on options for care and
treatment;
 immunization with the hepatitis A and B vaccines to
prevent coinfection from these hepatitis viruses to
protect their liver;
 early and appropriate medical management including
antiviral therapy if appropriate; and
 regular monitoring for early diagnosis of chronic liver
disease.