Presentation of AIDS

AIDS
INTRODUCTION
• Acquired immune deficiency syndrome(AIDS), It's caused by the human immunodeficiency virus, also
called HIV. HIV damages the immune system so that the body is less able to fight infection and disease
• Vital illness (a disease that can cause the patient to die).
• It breaks down the body’s immune system leaving the patient vulnerable to a host of life-threatening
opportunistic infections, neurological disorders, or unusual malignancies.
• Its incubation period is from a few months to 10 years
• Males>Females
• It occurs in all ages.
• AIDS is now the second leading cause of death for all men aged 25-44 years.
• About 37.9 million live with HIV and killed more than 35 million.
PREVALENCE
The prevalence of aids (acquired immunodeficiency syndrome) varies significantly by region and population
group. it is typically measured as the number of people living with aids per 100,000 population or as a
percentage of the population affected by the disease. here are some key points regarding the prevalence of aids:
• GLOBAL PREVALENCE: according to the World Health Organization (WHO), as of 2020, an estimated
38 million people worldwide were living with HIV/AIDS. the prevalence of aids varies widely by region,
with sub-Saharan Africa bearing the greatest burden of the epidemic.
• REGIONAL DISPARITIES: Sub-Saharan Africa has the highest prevalence of aids globally, with southern
Africa being the most affected region. In contrast, other regions such as North America, western and central
Europe, and parts of Asia have lower prevalence rates.
• POPULATION GROUPS: Certain population groups are disproportionately affected by HIV/AIDS,
including men who have sex with men, people who inject drugs, sex workers, transgender individuals, and
prisoners. Within these groups, prevalence rates may be much higher than in the general population
CAUSATIVE AGENT
It is caused by HIV (human immunodeficiency virus).
It has three stages:
Stage 1: Acute HIV
Some people get flu-like symptoms a month or two after they’ve been infected with HIV. These
symptoms often go away within a week to a month.
Stage 2: Chronic stage/clinical latency
After the acute stage, you can have HIV for many years without feeling sick. It's important to
know that you can still spread HIV to others even if you feel well.
Stage 3: AIDS
AIDS is the most serious stage of HIV infection. In this stage, HIV has severely weakened your
immune system, and opportunistic infections are much more likely to make you sick.
CONTINUE
the virus is spread (transmitted) person-to-person through certain body fluids:
• blood
• semen and pre-seminal fluid
• rectal fluids
• vaginal fluids
• breast milk
HIV can be spread if these fluids come in contact with:

• mucous membranes (inside of the mouth, penis, vagina, rectum)
• damaged tissue (tissue that has been cut or scraped)
• the bloodstream by injection
SYMPTOMS
• Persistent fever
• Fatigue
• Weight loss
• swollen lymph nodes
• Night sweats
• Recurrent infections
• Diarrhea
• Skin Rashes or Lesions
• Neurological Symptoms
• Mouth and Throat Problems
MECHANISM OF OCCURANCE
• BINDING gp-120 on the envelope of HIV binds to CD4 receptors together with co-receptor
CCR5 and CRX4.
• FUSION allows fusion of viral envelope with cell membrane which is facilitated by gp-41 then
fusion releases with virus contents.
• REVERSE TRANSCRIPTION We use reverse transcriptase enzyme which has a dual function
1st to make DNA double-strand complementary to RNA
2nd dissolve RNA and make another strand on DNA
After making the double-strand DNA virus it will be transported to the nucleus of the host cell.
• INTEGRATION INTEGRASE enzyme allows the integration of viral DNA with the host cell
DNA (by breaking the human DNA into two and then stitching the viral DNA into human DNA).
so now anytime the cell stimulates to produce its protein it will end up producing viral mRNA
then viral protein.
CONTINUE
and this protein has everything required for a virus to form and also to survive but the viral protein
has a single stretch that has to be cut into pieces to assemble a proper virus.
• TRANSCRIPTION IS where the host’s RNA polymerase reads the viral DNA with that
information it creates viral RNA as well as mRNA which will be used to create important proteins
of the virus.
• TRANSLATION is where mRNA that was just made is red by the host ribosomes to create a
protein that will essentially create enzymes and other proteins required to make a new HIV.
• ASSEMBLE AND RELEASE all these enzymes proteins and viral RNA are created assembled
packaged up and released by the cd4 cell.
• once CD4 T cell is released there is the final process of maturation where HIV uses its enzymes
to form its final infective
• Well, the virus replicates in the CD4 T cell and it injures the cell itself thus causing a slow
reduction in CD4 T cell.
TREATMENT
ANTIRETROVIRAL THERAPY
• CD4 BINDING INHIBITORS
Eg IBALIZUMAB ( it binds CD4 T cells thus inhibiting HIV from entering the cell)
• CCR5 INHIBITORS
Eg MARAVIROC (blocks ccr5 co-receptor that’s essential to cell infection)

• FUSION INHIBITORS
E.g. ENFUVIRTIDE (binds to viral protein GP-41 thereby preventing fusion virus envelope with the cell).
• REVERSE TRANSCRIPTASE INHIBITORS
it has two main types

1. NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBATORS
Essentially this drug works as a thymine analog they incorporate into the viral DNA and thus
terminate the DNA chain. Eg ABACAVIR
2. NUCLEOTIDE REVERSE TRANSCRIPTASE INHIBITORS
Adenosine nucleotide analog and again acts as a chain terminator when incorporated into viral
DNA. Eg TENOFOVIR. IT HAS TWO FORMS
Tenofovir disoproxil fumarate TDF AND Tenofovir alafnamide TAF
They differ in half-life and effects on kidneys and bones, and both are taken up from the gut when
you swallow the tab and act inside the cells to inhibit reverse transcriptase.
NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS
It binds directly to reverse transcriptase thus inhibiting its function rather than being an analog of some
nucleotide or nucleoside. Eg EFAVIRENZ
All reverse transcriptase inhibitors block and prevent DNA viral creation and therefore disrupt the
viral life cycle.
• INTEGRASE INHIBITORS
Inhibiting integration thus preventing the transfer and insertion of viral DNA to the host cell
DNA. Eg Raltegravir and dolutegravir.
• PROTEASE INHIBITORS
Designed to block the activity of protease enzyme, here causes the inability of the virus to cleave
certain proteins and activate them thus resulting in the generation of immature non-infectious
HIV.
The protease inhibitors required boosters such as ritonavir and cobicistat.
eg atazanavir and darunavir
PROPHYLAXIS FOR OPPORTUNISTIC INFECTION
prophylaxis for opportunistic infections in HIV patients involves the use of medications to prevent the
occurrence of specific infections that are more likely to affect individuals with compromised immune systems.
the choice of prophylactic medications depends on factors such as the patient's CD4 cell count, viral load,
previous history of opportunistic infections, and local guidelines. here are some common prophylactic
measures for opportunistic infections in HIV patients:
1. pneumocystis jirovecii pneumonia (pcp) prophylaxis:
1. trimethoprim-sulfamethoxazole (tmp-smx) is the preferred and most effective prophylactic agent for
pcp.
2. alternative agents for those allergic to tmp-smx include dapsone, atovaquone, or aerosolized
pentamidine.
2. tuberculosis (TB) prophylaxis:
1. isoniazid (INH) is the primary agent used for TB prophylaxis.
2. rifampin and rifabutin are alternative agents for those unable to tolerate INH.
Toxoplasmosis prophylaxis:
trimethoprim-sulfamethoxazole (tmp-smx) is also effective in preventing toxoplasmosis.
for patients intolerant to tmp-smx, alternatives include dapsone plus pyrimethamine plus
leucovorin.
cryptococcal meningitis prophylaxis:
fluconazole is often used for cryptococcal meningitis prophylaxis in patients with low cd4 counts.
cytomegalovirus (CMV) prophylaxis:
valganciclovir or oral ganciclovir may be used for CMV prophylaxis in certain high-risk HIV
patients.
bacterial infection prophylaxis:
antibiotics such as azithromycin or clarithromycin may be used for prophylaxis against bacterial
infections in patients with low cd4 counts.
when starting a patient with HIV treatment it is important to look out for (IRIS)
IMMUNE RECONSTITUTION SYNDROME (IRIS)
• immune reconstitution inflammatory syndrome is a clinical phenomenon that occurs after the
initiation of antiretroviral therapy. it represents a paradoxical worsening of preexisting infectious
processes following improvement in immune response and a subsequent state of elevated
inflammatory response. the preexisting infections can be subclinical (e.g. toxoplasmosis) or
previously treated infections (tuberculosis). the clinical presentation depends on the location and
severity of inflammation
• iris has been found to occur in up to 30 % of HIV/AIDS patients receiving ART.
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AIDS

HIV can be spread if these fluids come in contact with:

Eg MARAVIROC (blocks ccr5 co-receptor that’s essential to cell infection)

it has two main types

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