1. 4
José Aurelio Beltrán V.
José Manuel Yépiz Carrillo
José Luis Martínez Pérez
Paul Enrique López
UNIVERSIDAD DE SONORA
Licenciatura en Medicina

2. Human immunodeficiency
virus (HIV) is a blood-borne
virus typically transmitted
via sexual intercourse,
shared intravenous drug ,
and mother-to-child
transmission (MTCT), which
can occur during the birth
process or during
breastfeeding.
HIV disease is caused by
infection with HIV-1 or HIV-
2, which are retroviruses in
the Retroviridae family,
Lentivirus genus.

3. 1981 Centers for Disease
Control and Prevention (CDC)
Unexplained appearance
Pneumocystis Carinii,
1983 virus was isolated from
patients with lymph nodes.
1984 It was found that the
virus was the responsible
agent of AIDS.
1985 development of a test
that allowed realizing the
scope and evolution of the
epidemic infection.

5. Studies in the U.S. have
identified five high-risk
groups, distribution by
cases:
• Homosexuality or
bisexuality 50% of
reported cases.
• IV Drug without history
of homosexuality 20%
• Hemophiliacs, before
1985, 0.5%
• Blood transfusion,
hemophiliacs, 1%
• Heterosexual contact,
10%

7. "Extensive studies indicate that HIV infection cannot be transmitted
by personal contact. The spread by insect bites is impossible "

8. HIV disease is caused by
infection with HIV-1 or HIV-2,
both of which cause very
similar conditions. They differ
in transmission and
progression risks.
Human Retrovirus Family not
transforming
Lentivirus subfamily.
Two genetically distinct forms:
- HIV-1 (USA, Europe, Central Africa)
- HIV-2 (West Africa, India)

9. MorphologyStructures:
• It’s a spherical particle of 0.1 microns
• The viral core (or capsid): is usually
conical or bullet-shaped and is made from
the protein p24.
• The viral envelope (or membrane): it's
a lipid envelope derived from host cell
membrane that surrounding the core.
• The matrix: It´s just below the viral
envelope, which is made from the protein
p17 that cover the capsid directly.
Human Immunodeficiency Virus.

10. MorphologyComponents:
Inside the core
• p24: major capsid protein.
(viral antigen easier to detect)
• p7/p9: nucleocapsid protein.
• RNA genome, two copies.
• Viral enzymes (protease, reverse
transcriptase and integrase)
On the membrane
• Around 72 membrane complexes composed of…
• gp120 and gp41: glycoproteins that protrude viral coat.
That help HIV to enter the cell.
Human Immunodeficiency Virus.

12. Viral Genetic
gag. - Proteins of the capsid, RNA and matrix.
pol. - reverse transcriptase, protease and Integrase.
env. - surface membrane and transmembrane proteins.
Structural genes: contain information needed to make
structural proteins for new virus particles.
HIV has just nine genes (compared to more than 500 genes in a
bacterium, and around 20,000-25,000 in a human
HIV is a retrovirus of the lentivirus subgroup.

13. Viral Genetic
Accessory genes:
General functions:
1) Code for proteins that control the ability of HIV to infect a cell
2) Produce new copies of virus
3) Cause disease
How do they do? Synthesis and assembly product transactivators
Efect: increase 1000 times viral gene transcription

14. Viral Genetic
Vif.- Encodes a protein associated to virus infectivity
Tat.- Transactivator gene of proteins
Rev.- Regulator gene of the proteic exprecion viral
Nef.- Negative regulator (not proved )
Vpr.- Accelerator of cycle gene transcription and protein synthesis
Vpu.- Increases speeds of release virions (HIV-1 only)
Accessory genes:

15. Viral Genetic
At either end of each strand of RNA is a sequence called the
long terminal repeat, which helps to control HIV replication.
Grouped into regions of the envelope
glycoproteins, that is, in the env gene
Subgroups M, O and N.
Subtypes of Subgroup M are named as A - K.
Genomic variability

16. membrane
proteins.
Core and matrix
structure proteins.

17. Pathogeny of HIV infection
Severe loss of CD4
+ T lymphocytes
(helpers),
macrophages and
dendritic cells.
• Main Targets: Immune System and CNS.

18. Pathogeny of HIV infection
• HIV enters the body
through mucosal
tissues and blood.
• Infection is
established in
lymphoid tissues
where it can remain
dormant for an
extended period.

19. Cycle of the HIV
HIV can only replicate by invading the host cells , mainly
CD4 T lymphocytes
begins with the union of the membrane surface protein gp120 with the CD4 receptor of
T helper lymphocytes (also present in macrophages and dendritic cells ) .
There is a conformational change in gp120 , allowing it to bind to receptors CXCR4 and
CCR5 on the cell under attack. Finally, gp41 contributes to the union of the membranes.
Cycle of the HIV

20. Viral RNA is released into the host cell
The reverse transcriptase catalyzing
transcript of viral RNA to DNA
Viral DNA enters the nucleus and is
bound to the cell chromosomes by
integrase preferentially in areas of
major genetic expression.
Cell's DNA polymerase initiates
transcription of proviral DNA integrated
into the DNA of the cell , yielding a mRNA
Following transcription , the HIV mRNA is
translated into proteins which are
modified by glycosylation, myristylation,
phosphorylation and cleavage .
The viral particle is formed by the
assembly of proteins , enzymes and HIV
genomic RNA in the membrane of the
cell which formed the outer casing of
immature viron .
Protease ( coded by the virus before )
catalyzes the cleavage of gag-pol
precursor to yield the mature virion
Cycle of the HIV

23. Cytotoxic T lymphocytes.- HIV antigens induce exprecion
of cytokines such as IFN-y and lysis of infected cells
Proliferative cellular response.- Viral antigens induce the
proliferation of CD8 cytotoxic lymphocytes and NK
After the first viral outbreak in primary infection, it's
produces a solid immune response that determines the
slow development that characterize to HIV infection.
Immune response to HIVCellular

24. Neutralizing antibodies.- Are produced against
structural proteins gag gene (bases of diagnosis),
preventing binding of HIV to CD4 cells
Antibody dependent cellular cytotoxicity.-
When a phagocyte in contact with an infected cell
or HIV, opsonized; released cytokines that
collaborate in defense against infection
Humoral
Immune response to HIV

25. immune response to HIV

26. Clinical manifestations
• The clinical consequences of HIV infection
encompass a spectrum ranging from an acute
syndrome associated with primary infection to
a prolonged asymptomatic state to advanced
disease. It is best to regard HIV disease as
beginning at the time of primary infection and
progressing through various stages.

27. The Acute HIV Syndrome
• It is estimated that 50–70% of individuals with HIV
infection experience an acute clinical syndrome 3–6
weeks after primary infection
Opportunistic
infections have
been reported
during this stage of
infection, reflecting
the
immunodeficiency
that results from
reduced numbers of
CD4+ T cells and
likely also from the
dysfunction of CD4+
T cells

28. Clinical findings in Acute HIV Syndrome
Generals Especifics
-Fever -Meningitis
-Pharyngitis -Encefalitis
-Lymphadenopaty - Peripheral neuropathy
- Headache /retroorbital pain - Myelopathy
- Arthralgias / myalgias - Erythematous maculopapular rash
-Anorexia - Mucocutaneous ulceration
- Nausea/ vomiting / diarrhea

30. The Asymptomatic Stage (Latency)
• Although the length of time from initial
infection to the development of clinical
disease varies greatly, the median time for
untreated patients is 10 years.
• The rate of disease progression is directly
correlated with HIV RNA levels
• Patients with high levels of HIV RNA in plasma
progress to symptomatic disease faster than
do patients with low levels of HIV RNA
• During the asymptomatic period of HIV
infection, the average rate of CD4+ T cell
decline is 50/µL per year. When the CD4+ T
cell count falls to <200/µL, the resulting state
of immunodeficiency is severe enough to
place the patient at high risk for opportunistic
infection and neoplasms and, hence, for
clinically apparent disease.

31. Symptomatic Disease
• Symptoms of HIV disease can appear at any time during the
course of HIV infection
• Generally, the spectrum of illnesses that one observes
changes as the CD4+ T cell count declines
• The more severe and life-threatening complications of HIV
infection occur in patients with CD4+ T cell counts <200/µL
• Diagnosis of AIDS is made in anyone with HIV infection and
a CD4+ T cell count <200/µL  Indicate defect in cell-
mediated immunity

32. Diseases of respiratoy sistem
Acute bronchitis and sinusitis
Pulmonary disease (Pneumonia
and TB)
Fungal infections (coccidioides
immitis and aspergillus)
Neoplastic diseases (lymphoma)

33. Diseases of cardiovascular system
- Myocardial infarction
-Myocarditis
- Pericarditis
Patients with HIV infection have
higher levels of triglycerides,
lower levels of high-density
lipoprotein cholesterol

34. Diseases of oropharinx and
gastrointestinal system
-Aphtous ulcers
- Candida infections
- Leukoplakia
- Perirectal ulcers

35. Diseases of kidney and genitourinary tract
- Genitourinary tract infections
- Syphilis
- Vulvovaginal candidiasis

36. Diseases of hematopoietic system
-Lymphadenopaty
-Anemia
-Leukopenia
- Trombocytopenia
Can be the direct result of HIV,
manifestations of secondary
infections and neoplasms, or side
effects of therapy

37. Dermatologic diseases
- Folliculitis
- Reactivation herpes zoster
-Psoriasis
-Seborrheic dermatitis

38. Neurologic diseases
- Toxoplasmosis
- Cryptococcosis
-Trypanosomiasis
- Peripheral neuropathies
- Myopathy

39. Neoplastic diseases
- Kaposi’s sarcoma
-Lymphomas
- Burkitt’s lymphoma

40. Kaposi sarcoma and VIH
• It is the most common malignancy in patients
with SIDA.
• At the beginning of the epidemic, 30% of gay
or bisexual men were infected, today declined.
• Mushrooms. From fusiform smooth muscle
cells.
• Profusion of vascular spaces.
• chronic inflammatory cell infiltrates.
• affects homosexual men with AIDS 20 times
more often than male patients with hemophilia
and SIDA having a similar degree of
immunosuppression.

41. DIAGNOSIS

42. Screening test: the presence of antibodies to HIV in serum
or plasma , as evidenced by one of the following methods :
• - linked immunosorbent assay ( ELISA )
• - passive agglutination .
Additional Tests: presence of HIV antibodies in serum or
plasma.
• - blot ( Western blot test )
• - Immunofluorescence
• - Radioimmunoprecipitation ( RIPA )
Additional tests to determine the presence of
virus or any component
• - virus culture ;
• - determination of viral antigen ;
• - chain reaction of the polymerase, to determine the viral
RNA or proviral DNA .
Detection Procedure

43. Diagnosis of infection
• Detection in serum :
Anti - HIV antibody ELISA
test . With a sensitivity of
99.5 %. Detection of
antibodies and p24 antigen
are those with greater
sensitivity.
• Confirmation:
Western Blot: timely
assessment of the
specific reactivity of
antibodies to different
viral proteins.
When we do the study?
• When the person claims the study.
• Exposure to HIV infection
• unexplained Immunosuppression
• Pregnancy
• Son of a mother with HIV +
• Blood Donor

44. Person having two test results positive antibody screening and
supplemental testing positive, including asymptomatic patients
who refuse risk factors.
For present two screening test results positive, but further
evidence is indeterminate, should be considered as potentially
infected and so be informed , recommending repeat laboratory
diagnosis three months later.
Person positive zero

45. Treatment
a) Find a combination of highly
active antiretroviral drugs that are
capable of removing virtually HIV-1
replication.
b) allow the immune system is
reconstituted.
Reverse transcriptase inhibitors :
Zidovudine , Abacavir
Non-Nucleoside Inhibitors of Reverse
Transcriptase :
Efavirenz , Nevirapine
Protease Inhibitors :
Saquinavir, Indinavir

46. thanks for your attention