The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).

1. Human immunodeficiency virus
HIV is a lentivirus (a subgroup
of retrovirus) that causes HIV
infection and over time
acquired immunodeficiency
syndrome (AIDS)

2. Structure
• It is roughly spherical
• diameter of about 120 nm
• composed of two copies of positive-sense single-stranded RNA
• RNA codes for the virus's nine genes enclosed by a conical capsid composed of
2,000 copies of the viral protein p24
• RNA is tightly bound to nucleocapsid proteins- p7
• enzymes needed for the development of the virion such as reverse transcriptase,
proteases, ribonuclease and integrase are also present.
• A matrix composed of the viral protein p17 surrounds the capsid ensuring the
integrity of the virion particle
• A lipid viral envelope is present that composed of proteins like gp41 and gp120

3. Structure

4. Classification
• the International Committee on the Taxonomy of
Viruses (ICTV) as two separate families —
Papillomaviridae and Polyomaviridae.
• HPV is divided into High risk HPV and Low risk HPV. Low-
risk types cause warts and high-risk types can cause
lesions or cancer.

5. Pathogenesis
• HIV can infect immune cells such as CD4+ T cells,
macrophages, and microglial cells.
• HIV-1 entry to macrophages and CD4+ T cells is
mediated through interaction of the virion envelope
glycoproteins (gp120) with the CD4 molecule on the
target cells' membrane
• also with chemokine co-receptors – CCR5

6. Multiplication

7. Multiplication steps
Entry:
• The virion enters cells by the adsorption of gp on its surface to receptors (CD4,
CCR5) on the target cell
• followed by fusion of the viral envelope with the target cell membrane
• the release of the HIV capsid into the cell
Replication and transcription:
• reverse transcriptase liberates the positive-sense single-stranded RNA genome
from the attached viral proteins and copies it into a complementary DNA
(cDNA) molecule
Assembly and Release:
• The final step of the viral cycle, assembly of new HIV-1 virions, begins at the
plasma membrane of the host cell.

8. Multiplication steps
• The classical process of infection of a cell
by a virion can be called "cell-free
spread“
• In cell-free spread , virus particles bud
from an infected T cell, enter the blood
or extracellular fluid and then infect
another T cell following a chance
encounter.
• HIV can also disseminate by cell-to-cell
spread,

9. Symptoms
Primary HIV infection
• often is mistaken for influenza or a bad cold - reported by roughly half of those who
contract HIV
• generally occurs between 2 and 6 weeks after infection
• Symptoms may include fever, headache, sore throat, fatigue, body aches, weight loss,
and swollen lymph nodes. Neurological symptoms of peripheral neuropathy
• Other symptoms are a rash, mouth or genital ulcers, diarrhea, nausea and vomiting, and
thrush. Gastrointestinal symptoms, such as vomiting or diarrhea may occur
• The CD4+ T cell count can drop very low during the early weeks
• The initial illness can last several days or even weeks.
• The greatest spread of HIV occurs throughout the body early in the disease.

10. Symptoms
Latency period
• After initial infection comes the latency period, or incubation period
• period lasts a median of about 10 years.
• The most common symptom is lymphadenopathy, or swollen lymph
nodes.
• The lymph nodes of arms, neck, groin area

11. Symptoms
Acquired immunodeficiency syndrome (AIDS)
• defined in terms of either a CD4+ T cell count below 200 cells per µL or the
occurrence of specific diseases in association with an HIV infection.
• develop AIDS within ten years.
• most common initial conditions are pneumocystis pneumonia, cachexia in
the form of HIV wasting syndrome, and esophageal candidiasis and
recurrent respiratory tract infections
• increased risk of developing various viral-induced cancers, including
Kaposi's sarcoma, Burkitt's lymphoma, primary central nervous system
lymphoma, and cervical cancer.

12. Symptoms
Pulmonary
• Pneumocystis pneumonia (PCP) caused by Pneumocystis jirovecii a yeast like
fungus
• Tuberculosis (TB)
Gastrointestinal
• Esophagitis is an inflammation of the lining of the lower end of the esophagus
• Unexplained chronic diarrhea (Salmonella, Shigella, Listeria or Campylobacter)
Neurological
• Toxoplasmosis is a disease caused by the single-celled parasite called
Toxoplasma gondii
• demyelinating disease, in which the gradual destruction of the myelin sheath
covering the axons of nerve cells impairs the transmission of nerve impulses
(by JC virus)
• Dementia
Tumors
• Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients
• Lymphoma, cervical cancer, hepatocellular carcinoma

13. Transmission
• Only certain body fluids—blood, semen, pre-seminal fluid, rectal fluids,
vaginal fluids, and breast milk
• from a person who has HIV can transmit HIV.
• These fluids must come in contact with a mucous membrane or
damaged tissue
• or be directly injected into the bloodstream (from a needle or syringe)
for transmission to occur.
• Mucous membranes are found inside the rectum, vagina, penis, and
mouth.

14. Transmission
You can get HIV via..

15. Transmission
• Sex without a condom:
having unprotected sex with someone who has HIV, particularly unprotected vaginal sex and anal
sex.
• Sharing injecting equipment:
sharing needles, syringes or other equipment used to prepare and inject drugs with someone who
has HIV.
• Passed from mother-to-baby during pregnancy, childbirth and breastfeeding
a mother infected with HIV can pass the virus to her baby via her blood during pregnancy and
birth, and through her breast milk when breastfeeding.
• Contaminated blood transfusions and organ/tissue transplants
receiving blood transfusions, blood products, or organ/tissue transplants that are contaminated
with HIV. This risk is extremely small because most countries test blood products for HIV first.

16. Diagnosis: ELISA TEST
• An enzyme-linked immunosorbent assay (ELISA) is a test that
uses enzymes and colour changes to identify a substance
• It can be used to identify specific surface markers or
metabolites associated with particular diseases
• Different variations of the ELISA test exist, but one of the
most common protocols involves the sandwich method:

17. Diagnosis: ELISA TEST
• Known monoclonal antibodies are
affixed to wells in a plate (these are
the 'capture antibodies')
• A sample to be tested is added to the
wells and any antigens present will
bind to the appropriate capture
antibody
• The plates are then washed to remove
any unbound antigen

18. Diagnosis: ELISA TEST
• A second set of monoclonal antibodies linked to
colour-changing enzymes are then added to the wells
• These 'detection antibodies’ will bind to any antigens
captured, creating a sandwich (antibody - antigen -
antibody)
• The wells are then washed again to remove any
unbound detection antibodies
• When an appropriate substrate is added to the wells,
the enzyme-linked detection antibodies will trigger a
colour change

19. Diagnosis: ELISA TEST

20. Diagnosis:
Common diagnosis methods are ELISA testing, but has to e confirmed by PCR
or NAT or Western blot
• ELISA testing
• Western blotting
• nucleic acid testing (NAT)
• Polymerase chain reaction

21. Pre Exposure Prophylaxis
PrEP is a single daily
pill of trivada (drug
combination of
tenofovir/emtricitabi
ne) that can reduce
risk of HIV by up to
90%
PrEPis an option for all
genders who are
HIV-negative and
at risk for HIV
PrEP does not
prevent STIs or
pregnancy. PrEP is
more effective when
it is combined with
other prevention
measures like
condoms

22. Post Exposure Prophylaxis
PEP means taking
antiretroviral
medicines (ART) after
being potentially
exposed to HIV to
prevent becoming
infected with in
72hrs for
28days
PEPis an option for all
genders who are
HIV-negative and
at risk for HIV
PEP does not
prevent STIs or
pregnancy. You
should continue to
use condoms with
sex partners and
safe injection
practices while
taking PEP

23. Treatment
• Treatment consists of highly active antiretroviral therapy (HAART) which slows
progression of the disease.
• Current HAART options are combinations consisting of at least three
medications belonging to at least two types of antiretroviral agents
• typically a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two
nucleoside analog reverse transcriptase inhibitors (NRTIs).
• zidovudine (AZT) or tenofovir (TDF) and lamivudine (3TC) or emtricitabine
(FTC)
•

24. Treatment
• Once treatment is begun it is recommended that it is continued without
breaks
• treatment with antiretrovirals reduces the risk of developing additional
opportunistic infections
• Dietary intake of micronutrients
• higher intake of vitamin A, zinc, and iron can produce adverse effects in HIV
positive adults, and is not recommended unless there is documented
deficiency

25. Ocular Manifestations of HIV
• The institution of highly active antiretroviral therapy (HAART) has caused a dramatic
improvement in the immune status of HIV-infected individuals and a change in the clinical
presentation and course of opportunistic infections
• However, the benefits of HAART may be attenuated by the development of immune recovery
uveitis (IRU), which is characterized by intraocular inflammation (commonly intermediate
uveitis or a combination of anterior and intermediate uveitis), in conjunction with immune
recovery, and may be associated with ocular complications such as cataract, cystoid macular
edema (CME), and epiretinal membrane (ERM) formation
• A proposed pathogenesis for IRU is that immunologic improvement in response to HAART
causes the restoration of specific anti-CMV immunity, which leads to an inflammatory
response directed at the CMV antigen present in the eye
• Immune recovery uveitis may occur soon after initiating HAART (less than 1 month), but also
has been reported to occur as long as 3 years after starting HAART.

26. Ocular Manifestations of HIV
• herpes zoster ophthalmicus (HZO): a dermatitis with vesicles and blisters in the division
of the trigeminal nerve caused by the Varicella zoster virus (VZV)
• 5% to 15% of HIV patients and may be associated with a simultaneous occurrence of
keratitis, scleritis, uveitis, retinitis, or encephalitis
• Kaposi sarcoma is a highly-vascularized, mesenchymal tumor and may present as painless,
violaceous lesions on the eyelid skin or conjunctiva
• Molluscum contagiosum is a dermatitis caused by a poxvirus and characterized by
multiple, small, painless umbilicated lesions on the eyelid skin
• 80% of HIV patients may present with conjunctival microvasculopathy, characterized by
segmental dilatation and narrowing of blood vessels, comma-shaped vascular segments,
and sludging of blood column
Other HIV related infection

27. Ocular Manifestations of HIV
• Posterior segment involvement in HIV is quite common and can cause visual loss
• They include Retinal microangiopathy, CMV retinitis, VZV retinitis, toxoplasma
retinchoroiditis, and bacterial and fungal retinitis
• Keratoconjunctivitis sicca, or dry eyes, are seen in approximately 20% of HIV patients and
are thought to be an HIV-mediated inflammatory destruction of lacrimal glands
• Keratitis in HIV is rare, seen in less than 5% of cases, but can lead to loss of vision. Herpes
simplex virus and varicella-zoster virus are the most common causes
• Orbital involvement is rare in HIV and includes orbital lymphoma and orbital cellulitis,
usually caused by Aspergillus
Posterior segment involvement in HIV

28. Ocular Manifestations of HIV
• Treatment of the ocular manifestation depends upon the presenting ocular pathology
• Treatment of Herpes zoster ophthalmicus includes systemic acyclovir, famciclovir,
valacyclovir and, in resistant cases, intravenous foscarnet
• Kaposi sarcoma is managed by radiation therapy and institution of HAART therapy
• Molluscum contagiosum can be treated by cryotherapy, curettage, and surgical excision
• Treatment of Keratoconjunctivitis sicca includes artificial tears and long-acting lubricants
• Keratitis is treated depending on the cause: viral keratitis by oral acyclovir or famciclovir;
microsporidial keratitis by oral itraconazole, topical fumagillin, and oral albendazole;
bacterial and fungal keratitis with appropriate antimicrobial therapy.
Treatment of the ocular manifestation