This document provides an overview of AIDS/HIV, including its etiology, pathogenesis, diagnosis, and treatment. It is caused by the HIV virus, which destroys CD4+ T cells. It discusses the life cycle and structure of HIV, how it is transmitted, and the role of key enzymes like reverse transcriptase. Diagnosis involves blood or urine tests to detect HIV antibodies. Treatment involves antiretroviral drugs that target different stages of the viral life cycle, such as reverse transcriptase inhibitors, protease inhibitors, and integrase inhibitors. Vaccine development and other new therapies like gene and monoclonal antibody therapies are also discussed.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).
HIV infection
Mode of transmission, pathogenesis, clinical manifestations, laboratory diagnosis, treatment, prevention, prognosis, scope of AIDS vaccine.
The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).
HIV infection
Mode of transmission, pathogenesis, clinical manifestations, laboratory diagnosis, treatment, prevention, prognosis, scope of AIDS vaccine.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Pulmonary TB is a bacterial infection of the lungs that can cause a range of symptoms, including chest pain, breathlessness, and severe coughing. Pulmonary TB can be life-threatening if a person does not receive treatment. People with active TB can spread the bacteria through the air.
Immunity is the ability of the body to protect against all types of foreign bodies like bacteria, virus, toxic substances etc. As it protects us from diseases it is also called disease resistance. Immunity is done by immune system which is a complex network of lymphoid organs such as bone marrow, thymus, spleen etc. It is mainly of two types- Natural and Acquired immunity.
Chronic obstructive pulmonary disorders COPD is a [preventable and treatable disease with some significant extra pulmonary effects that may contribute to the severity in individual clients.
It is characterized by airflow limitation that is not completely reversible.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Pulmonary TB is a bacterial infection of the lungs that can cause a range of symptoms, including chest pain, breathlessness, and severe coughing. Pulmonary TB can be life-threatening if a person does not receive treatment. People with active TB can spread the bacteria through the air.
Immunity is the ability of the body to protect against all types of foreign bodies like bacteria, virus, toxic substances etc. As it protects us from diseases it is also called disease resistance. Immunity is done by immune system which is a complex network of lymphoid organs such as bone marrow, thymus, spleen etc. It is mainly of two types- Natural and Acquired immunity.
Chronic obstructive pulmonary disorders COPD is a [preventable and treatable disease with some significant extra pulmonary effects that may contribute to the severity in individual clients.
It is characterized by airflow limitation that is not completely reversible.
Introduction to HIV/AIDS
Epidemiology
Structural information of HIV
Life cycle of HIV
Symptoms & causes of AIDS due to HIV
Pathophysiology
Pharmacological Classification along with mechanism of action
Novel targets for Anti-retroviral Drugs
Summary
References
Vote of thanks
HIV is a lentivirus which can not only infect actively dividing cells but also non-dividing cells such as macrophages. AIDS is the last stage of HIV infection. HIV primarily attacks T- helper cells resulting into low activated T-cytotoxic cells and suppression of immune system. thus leading to AIDS.
Etiology, pathophysiology, Pharmacotherapy of AIDS .pptxdrsriram2001
Definition of AIDS:
Acquired Immunodeficiency Syndrome (AIDS) is a late stage of HIV (Human Immunodeficiency Virus) infection. It is characterized by a severe depletion of the immune system, making the individual susceptible to opportunistic infections and certain cancers.
2. Etiology (HIV):
HIV Structure:
HIV is a retrovirus that primarily targets CD4+ T cells, a crucial component of the immune system.
The virus has two main types: HIV-1 and HIV-2, with HIV-1 being the most common and virulent worldwide.
3. Transmission:
Modes of Transmission:
HIV is primarily transmitted through unprotected sexual intercourse with an infected person.
It can also be transmitted through sharing of contaminated needles, from an infected mother to her child during childbirth or breastfeeding, and through blood transfusions with infected blood (though this is rare now due to blood screening).
4. Clinical Stages:
Acute HIV Infection:
Occurs within the first few weeks after exposure.
Presents with flu-like symptoms such as fever, fatigue, and swollen lymph nodes.
Chronic HIV Infection (Asymptomatic Stage):
Can last for several years with few or no symptoms.
The virus is actively replicating, and the immune system is gradually compromised.
Symptomatic HIV Infection (Symptomatic Stage):
As the immune system weakens, symptoms such as persistent fever, weight loss, and diarrhea may occur.
AIDS:
Diagnosed when the immune system is severely compromised, typically when the CD4+ T cell count falls below a critical threshold.
Opportunistic infections (e.g., Pneumocystis jirovecii pneumonia) and certain cancers (e.g., Kaposi's sarcoma) become more common.
5. Preventive Measures:
Condom Use:
Consistent and correct use of condoms during sexual intercourse helps prevent the sexual transmission of HIV.
Pre-Exposure Prophylaxis (PrEP):
Antiretroviral medications, when taken consistently by HIV-negative individuals at high risk, can prevent HIV infection.
Post-Exposure Prophylaxis (PEP):
Emergency treatment with antiretroviral drugs within 72 hours of potential exposure to HIV to prevent infection.
Needle Exchange Programs:
Reducing the sharing of needles among injecting drug users helps prevent the transmission of HIV.
A LECTURE ON AIDS FOR FIRST MBBS STUDENTS, DEPT OF BIOCHEMISTRY.
A CLASS ON EPIDEMIOLOGY, VIROLOGY,HIV-MORPHOLOGY, GENOME, LIFE CYCLE,MODE OF TRANSMISSION, IMMUNOLOGY, PATHOPHYSIOLOGY AND PATHOGENESIS, LABORATORY DIAGNOSIS AND MANAGEMENT.
MANAGEMENT OF HIV FALLS UNDER THREE MAJOR CATEGORIES
1.POST EXPOSURE PROPHYLAXIS(P.E.P)
2.TREATMENT/MANAGEMENT OF HIV-AIDS
3.TREATMENT OF ADJOINING CONDITIONS
eg-
-Fungal Infections
-Bacterial infections
-Viral infections
-NEOPLASIAS
-misc.( recurrent apthos ulcers, xerostomia,salivary G. enlargement)
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3. Introduction
• AIDS- Acquired Immunodeficiency Disease.
• It is a disease caused by the retrovirus human
immunodeficiency virus (HIV) and characterized by
profound immunosuppression that leads to
opportunistic infections, secondary neoplasms and
neurological manifestations.
• The acquired immune deficiency syndrome AIDS was
first recognized in 1981 in US.
• Centers for Disease Control and Prevention reported
the unexplained occurrence of Pneumocystis jiroveci
pneumonia in five previously healthy homosexual
men in Los Angeles and of Kaposi's sarcoma with or
4. without P. jiroveci pneumonia in 26 previously healthy
homosexual men in New York and Los Angeles.
ETIOLOGY
• AIDS is caused by HIV, a human retrovirus.
• Two types- HIV I and HIV II which are genetically
different but has related forms.
• HIV I is most common type associated with AIDS in
US, Europe and Central Africa.
• HIV II causes similar disease in West Africa and India.
• HIV-II is transmitted less efficiently than HIV-I.
5. STRUCTURE
• HIV is a typical retrovirus with a small RNA genome
of 9300 base pairs.
• Is a spherical and contains nucleocapsid core
surrounded by a lipid bilayer or envelop derived from
host cell membrane.
• The viral genome encodes 3 major open reading
frames-
1. gag encodes a polyprotein that is processed to
release major structural proteins of virus.
2. pol encodes 3 important enzymes are RNA
dependent DNA polymerase or reverse
transcriptase with RNAse H, Protease and integrase.
6. 3. env encodes for large transmembrane envelop
proteins responsible for cell binding and entry.
• Several small genes encodes regulatory proteins
that enhances virion production or combat host
defence.
7. PATHOGENESIS
• HIV can infect many tissues, there are 2 major targets
-Immune system
-Central nervous system.
• Primarily affect cell mediated immunity.
• Results in severe loss of CD4+ T cells and impairment
in the function of helper T cells.
• Macrophages and dendritic cells also infected.
8. LIFE CYCLE OF HIV
• STEP’S INVOLED
1.INVASION
a) Attachment
b) Fusion
2.MATURATION
a) Reverse transcriptase
b) Integration
3.RELEASE
a) Budding
b) Exit from cell
9. ROLE OF ENZYMES
1. REVERSE TRASCRIPTASE (RT)
• Multifunctional enzymes having RNA
dependent DNA polymerase activity
• Also having RNase H (helicase) activity
• Catalyses formation of double stranded
proviral DNA from singal stranded RNA
genome
• Due to its central role in the viral replication
RT is prime target for anti aids therapy
10. • Inhibitors of RT can be classified as
1.nucleoside RT inhibitor(NRTI)
2.non nucleoside RT inhibitor(NNRTI)
• NRTI are competative in nature while NNRTI
are non competative
2. PORTEASE
• Protease essential for production of mature,
infectious virions
• HIV protease is responsible for posttranslatio-
nal processing of poly proteins & protolytic
activity
11. • Inhibition of these protease enzyme is also
attractive target for anti aids therapy
3. Intigrase
• Catalyses the integration of double stranded
DNA copy of their RNA genome into
chromosome of a host cell
• Inhibition of integrase enzyme is prime target
for anti aids therapy
12. COMMAN SIGN & SYMPTOMS
• Severe impairment or suppression of immune
system.
• Pneumocystis carinii pneumonia (pcp) is
mostly seen.
• Opportunistic infection
• CD4+T- cells count falls below 200 cells/mm3
of blood.
• In healthy adult it’s value is 600-1500
cells/mm3 of blood.
15. Through Bodily Fluids
• Semen
• Vaginal fluids
• Breast Milk
HIV enters the bloodstream through
– Open Cuts
– Breaks in the skin
– Mucous membranes
– Direct injection
16. • Sharing Needles
– Without sterilization
Through Sex
• Intercourse
• Oral
• Anal
Mother-to-Baby
• During pregnancy transplacently transmitted.
• During post-partum period through contamination
with maternal blood, infected amniotic fluid or
breast milk
17. DIAGNOSIS
BLOOD DETECTION TEST
• Enzyme-Linked Immunosorbent Assay/Enzyme
Immunoassay (ELISA/EIA)
• Radio Immunoprecipitation Assay/Indirect
Fluorescent Antibody Assay (RIP/IFA)
• Polymerase Chain Reaction (PCR)
• Western Blot Confirmatory test
18. URINE TEST
• Urine Western Blot
• As sensitive as testing blood
• Safe way to screen for HIV
• Can cause false positives in certain people at
high risk for HIV
Orasure
– The only FDA approved HIV antibody.
– As accurate as blood testing
– Involves collecting secretions between the cheek
and gum and evaluating them for HIV antibodies.
21. NUCLEOSIDE/NUCLEOTIDE ANALOGUES
• Nucleoside and nucleotide reverse
transcriptase inhibitors prevent infection of
susceptible cells but have no impact on cells
that already harbor HIV.
• Nucleosides that must be triphosphorylated at
the 5’-hydroxyl to exert activity.
• tenofovir, is a nucleotide monophosphate
analog that requires two additional
phosphates to acquire full activity.
22. ZIDOVUDINE:
• 3’ azido- 3’ deoxythymidine.
• Synthetic thymidine analogue with potent
broad spectrum activity.
Mechanism of Action:
• due to similar structure
it incorporate in to growing
DNA strand and terminate
synthesis due to lack of
OH group.
23.
24. Untoward Effects
• They mainly due to partial inhibiton of cellular
DNA polymarase.
• Fatigue, malaise, myalgia, nausea, anorexia,
headache, and insomnia.
• Bone marrow suppression, mainly anemia and
granulocytopenia.
• Gastrointestinal disturbances
• Abnormal liver functions
• hyperlipidemia
25. Therapeutic Uses.
• Zidovudine is FDA approved for the treatment
of adults and children with HIV infection and
for preventing mother-to-child transmission of
HIV infection.
• It is also recommended for postexposure
prophylaxis in HIV-exposed healthcare
workers, also in combination with other
antiretroviral agents.
26. NONNUCLEOSIDE REVERS TRANSCRIPTASE
INHIBITORS
• Nonnucleoside reverse transcriptase inhibitors
(NNRTIs) include a variety of chemical
substrates that bind to the HIV-1 reverse
transcriptase.
• These compounds induce a conformational
change in the three-dimensional structure of
the enzyme that greatly reduces its activity,
and thus they act as noncompetitive inhibitors
27. NEVIRAPINE:
• Is a dipyridodiazepinone NNRTI with potent
activity against HIV-1.
• nevirapine does not have significant activity
against HIV-2 or other retroviruses.
Mechanism of Action:
• Nevirapine is a noncompetitive inhibitor that
binds to a site on the HIV-1 reverse
transcriptase that is distant from the active
site, inducing a conformational change that
disrupts catalytic activity.
28.
29. Untoward Effects:
• Hepatotoxicity
• Stevens-Johnson syndrome
• Rash
• Pruritus
• Fever, fatigue, headache, somnolence, and
nausea.
Uses
• Pregnant women
• Used to prevent mother to infant HIV infection
• HIV-1 infection in adults and children in
combination with other antiretroviral agents.
30. PROTEASE INHIBITORS
• HIV protease inhibitors are peptidelike
chemicals that competitively inhibit the action
of the virus aspartyl protease.
• This protease is a homodimer consisting of
two 99-amino-acid monomers; each monomer
contributes an aspartic acid residue that is
essential for catalysis.
31. SAQUINAVIR:
• A peptidomimetic hydroxyethylamine HIV
protease inhibitor.
• Inhibits both HIV-1 and HIV-2 replication.
Mechanisms of Action
• Reversibly binds to the active site of HIV
protease, preventing polypeptide processing
and subsequent virus maturation.
• Potently inhibiting the HIV-encoded protease
but not host-encoded aspartyl proteases.
32. Untoward Effects
• Nausea, vomiting, diarrhea, and abdominal
discomfort.
• Lipodystrophy.
Therapeutic Use
• Reduction of viral load with other nucletide
analogues.
33. FUSION INHIBITORS
• Enfuvirtide is the only available HIV entry
inhibitor.
• Enfuvirtide is a 36-amino-acid synthetic
peptide whose sequence is derived from a
part of the transmembrane gp41 region of
HIV-1.
• Not active against HIV-2.
• The peptide blocks the interaction between
the N36 and C34 sequences of the gp41
glycoprotein by binding to a hydrophobic
groove in the N36 coil
34. • This prevents formation of a six-helix bundle
critical for membrane fusion and viral entry
into the host cell.
• Treatment-experienced adults who have
evidence of HIV replication despite ongoing
antiretroviral therapy.
35. CCR5 antagonists
• In order to enter a human cell, HIV must first
attach itself to proteins on the cell’s surface.
• The next stage involves proteins called co-
receptors, two main types: CCR5 and CXCR4.
Some strains of HIV use CCR5, others use
CXCR4,.
• CCR5 antagonists are drugs that bind to the
CCR5 co-receptor so that HIV cannot exploit it
to gain entry to a cell.
• The main drawback of these drugs is that they
don’t work against all strains of HIV.
• Maraviroc is a example for this class.
36. Raltegravir: first in class HIV integrase inhibitor
• The integration of HIV-1 proviral DNA into the
host cell genome
• Integrase mainly involved in integration of
viral DNA in to host DNA.
• Inhibition of this enzyme prevents integration.
• Impressive antiviral potency in heavily
treatment-experienced patients.
37. RECENT THERAPY FOR AIDS
Drug class Recently approved Phase III Phase II
Entry inhibitor
Maraviroc (Aug. 2007) Vicriviroc PRO 140
(CCR5)
Entry inhibitor (CD4) TNX-355
Integrase inhibitor Raltegravir (Oct. 2007) Elvitegravir
Maturation inhibitor Bevirimat
NNRTI Etravirine (Jan. 2008) Rilpivirine
KP-1461
NRTI Apricitabine Racivir
Elvucitabine
38. GENE THERAPY
• RNA-interference is damage to a certain RNA
sequence with participation of a different,
"defending" RNA molecule.
• This system prevents viral infection, unless
viruses had learned to cut it off in the course of
evolution.
• Researchers from countries including Russia are
developing the artificial RNA-interference system.
• It is non-injurious to the patient and, due to high
specificity of action, does not damage its own
RNA in cells infected by the virus.
39. • To fight HIV, Russian biologists have created
three genetic structures.
• These structures contain short nucleotide
against sequences that find the most
conservative molecules among all RNA
molecules, that is, sequences that do not
change quickly and are important to the virus.
• These sequences are then "damaged".
• Genetic structures significantly suppress viral
reproduction.
40. VACCINE
Difficulties in developing an HIV vaccine
• Classic vaccines mimic natural immunity against
reinfection generally seen in individuals
recovered from infection; there are almost no
recovered AIDS patients.
• Most vaccines protect against disease, not against
infection; HIV infection may remain latent for
long periods before causing AIDS.
• Most effective vaccines are whole-killed or live-
attenuated organisms; killed HIV-1 does not
retain antigenicity and the use of a live retrovirus
vaccine raises safety issues.
41. • Most vaccines protect against infections
through mucosal surfaces of the respiratory or
gastrointestinal tract; the great majority of
HIV infection is through the genital tract.
Phase I
• Most initial approaches have focused on the
HIV envelope protein.
• Thirteen different gp120 and gp160 envelope
candidates have been evaluated.
• Most research focused on gp120 rather than
gp41/gp160.
42. Phase III
• AIDSVAX vaccine.
• This is the first successful HIV vaccine trial in
history.
• The percentage rate reduced to 26%
compared with those who had been given a
placebo.
Planned clinical trials
• Novel approaches, including modified vaccinia
Ankara (MVA), adeno-associated virus,
Venezuelan equine encephalitis (VEE).
43. MONOCLONAL ANTIBODIES
• monoclonal antibodies, produced after
immunizing mice, have binding characteristics
that look similar to two well-known broadly
neutralizing human monoclonal antibodies,
known as 2F5 and 4E10, which also bind to
HIV-1 protein and lipid.
• That might be useful in an effective HIV-1
vaccine.
44. REFERENES
1. The Pharmacological basis of Therapeutics by
Goodman and Gilman’s, 11 ed.
2. Pathologic basis of disease by Robbins and
Cotran, 7 ed.
3. Pharmacology by Rang and Dale’s, 6 ed.
4. www.google.com