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Desiree Campos

on 17 August 2015

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Transcript of HIV/AIDS

Desiree Campos
HIV Stages and Symptoms
Opportunistic infections and cancers
What is HIV/AIDS?
History of HIV
-Infection stage vs disease stage
First appear as flu like symptoms:
Sore throat
Muscle aches
Enlarged lymph nodes
Decreased appetite
HIV is the Human Immunodeficiency Virus
Immunodeficiency disorders impair the immune systems ability to defend against foreign agents.
HIV is classified as a Retrovirus and in the sub group of Lentiviruses.

HIV is a Chronic infection.
Why are Chronic infections most difficult to control within a population?
Improper usage of condoms
Mucosa membranes

Semen, cervical and vaginal secretions
Organ transplants
Medical equipment
Unsterilized needles (piercings, tattoos, etc.)
Sharing needles

Breast milk
(In utero) via placenta
Vertical precautions
Not breast feeding, cesarean section, and taking Antiretroviral treatment (ARV)

HIV Stages
Causative agents
Preliminary diagnostic questions

(Step 1) Clinical testing
Finger stick
Blood draw
Cheek swab
(Step 2) Confirmation testing
Western blot test

Properly use latex condoms

HIV screening

Don’t share needles of any sort

Treat all blood products as if they are infected
Every person will experience the
each stage of HIV/AIDS differently in terms of symptoms and duration
(Anderson et al, 2012)
(Anderson et al, 2012)
(Merck Manual of Medical Information, 2004)
Stage 3: Symptomatic infection
(Judd, 2011)
What is HIV?
(Anderson et al, 2012)
(Anderson et al, 2012)
(Anderson et al, 2012)
(Anderson et al, 2012)
(Anderson et al, 2012)
(Merck, 2012)
(Anderson et al, 2012)

Acquired immunodeficiency syndrome

In the United States, AIDS is the leading cause of death for individuals aged 25-44

AIDS onset may be estimated by tracking viral loads and CD4+ cell counts

What is a normal CD4+ cell range for non infected individuals in good health?
What happens when a person's CD4+ count falls below 200/mm?

HIV: a global perspective 2011
HIV can still be transmitted even if the infected party is asymptomatic
(Moore, 2007)
-Democratic republic of congo 1959.
- St. Louis teen 1969.
-Unknowingly mass transmitted in 1950's.
-Blood bank epidemic 1981-1985.
-Brought to the attention of world in 1980's.
-Initially described as a rare pneumonia or cancer.
-Robert Gallo and Luc Montegnier.

(WHO, 2011)
What are the implications?
supply, demand, and cost

Children living with HIV
(Conner, Fan & Villarreal, 2007 )
HIV in the U.S.
Acute vs chronic infection
(Judd, 2011)
Each year, 28,000 Men are infected.
Each year, 12,000
Women are infected.
Each year, HIV infects 40,000 people; 30% of which are women and 70% are men.
1 in 2
Mothers not being properly treated with ARVs will transmit HIV to their baby.

1 in 4
Mothers properly being treated with ARVs will transmit HIV to their baby.

HIV 1 groups
Major group
Outlier group
New groups

Within 2-4 weeks of transmission, acute or primary HIV infection occurs
can occur when an individual is exposed to differing strains of HIV near simultaneously.

Can one be infected with
multiple strains of HIV?
Super infection
may occur when an individual is infected a second time several months after the initial infection.
Structure of HIV
gp41: T
ransmembrane glycoprotein

Surface glycoprotein
P6: a core protein allows budding to occur from the host cell.

P17: a structural matrix protein.

P24: is a viral core protein located within the viral capsid consisting of 2000 copies.

surrounds 2 single strands of RNA (each containing 9 genes).
(Anderson et al, 2012)
RT enzyme:
copies viral RNA to DNA.
(Anderson et al, 2012)
Viral Envelope:

lipid bi-layer with about 72 glycoprotiens.
(Anderson et al, 2012)
Virion structure
(Avert, n.d.).
PR enzyme:
viral protein processing
IN enzyme:
inserts viral cDNA
into host cell

CD4+ Helper T-cells
Produce receptors that recognize specific antigens
T-cells then bind to foreign agents via the receptors

CD8+ Cytotoxic Cells
Secrete soluble factors that suppress HIV replication
Attack and kill HIV infected cells
Dendritic cells
Located in mucosa.
Carry the virus to the lymph nodes.
Significance of the DC-SIGN molecule.
Macrophages and Monocytes are fairly resistant-- however, they travel throughout the body carrying the virus to various organs.
'(Turbosquid, 2013)
1 in 2 HIV infected
individuals endure

neurological manifestations
The miraculous immune system

Lymphnodes act as army barracks for WBCs
B cells are like drones
Helper B and T cells act as military command and control
Dendrons serve as surveillance
In the words of Sam Shabb...
(Anderson et al, 2012)
(Judd, 2011)
(Judd, 2011)
(Cosmos, 2007)
(Judd, 2011)
(Anderson et al, 2012)
(Conner, Fan & Villarreal, 2007)
(Conner, Fan & Villarreal, 2007)
(Judd, 2011)
(Judd, 2011)
(Judd, 2011)
T- Lymphocytes
(The Body Pro, 2003)
B - Lymphocytes

Secrete antibodies
Once an antibody binds to an antigen, the immune system attacks.
Neutralizing antibodies inhibit infectious agents.
(Conner, Fan & Villarreal, 2007)
(Conner, Fan & Villarreal, 2007)
(AIDS.gov, 2012)
HIV replicates rapidly
HIV reverse transcriptase enzyme makes many errors during transcription
(Connexions, 2013)
What cells are affected?
There are multiple contributing factors to disease progression and severity per stage.
Acute infection phase
Chronic infection phase
Rapid progression
weeks of infection most of an individual's CD4+ cells have been lost.
Subtypes with in Group M
Circulating recombinant forms (CRFs)
(Judd, 2011)
What is the potential risk of more HIV subtypes appearing?
Lymphatic Circulation
Upon viral infection, virus particles are transported down the lymph channels and ultimately end up in the bloodstream.
CD4+ T cells loses their ability to produce Interluekin-2
HIV facilitates apoptosis or programmed cell suicide.
-Uninfected cells
-Infected cells
HIV has the ability to disturb the microenvironment of bone marrow and the thymus
HIV can go undetected in the human body simply due to its structure
HIV replicates rapidly
(Judd, 2011)
(Kuitkuppala 2009)
(Anderson et al, 2012)
(Judd, 2011)
(Judd, 2011)
(Judd, 2011)
(Conner, Fan & Villarreal, 2007)
(Judd, 2011)
Chronic immune system activation
(Judd, 2011)
(Judd, 2011)
(Judd, 2011)
Who is at risk for super infection?

What are the implications?
(Judd, 2011)
Stage 1: Primary infection
Duration of a few weeks
Accompanied by flu-like symptoms
The immune system begins responding to the large amount of HIV in the blood
(Judd, 2011)
Stage 2: Clinically asymptomatic
HIV remains very active
although the level of HIV in peripheral blood has dropped significantly
Duration can last up to about 10 years
(Judd, 2011)
(Judd, 2011)
Immune system has become severely damaged
Lymphnodes and tissues are ravaged
HIV mutates becoming more pathogenic
The body can no longer adequately replace T cells as they are lost
Symptoms worsen as the immune system continues to fail
Opportunistic infections emerge
(Brenchly, 2004)
Respiratory system
Kaposi Sarcoma
Gastrointestinal system
Central/peripheral nervous system
Non-Hodgkin Lymphoma
Herpes simplex
Varicella Zoster

Home rapid testing is a quick alternative to clinical testing

However, if the test indicates a positive result one should seek clinical testing.
(Anderson et al, 2012)
(Judd, 2012)
Acute Retroviral Syndrome
Without treatment, HIV typically progresses to AIDS in 10-12 years.
Antiretroviral drugs suppress the viral load by interrupting the HIV life cycle

Types of ARV drugs:
Protease inhibitors
Nucleoside reverse transcriptase inhibitors
Integrase inhibitors
Non-nucleoside reverse transcriptase inhibitors
Entry inhibitors
Nucleotide analog reverse transcriptase inhibitors
(Conner, Fan & Villarreal, 2007)
Strict adherence to ARV medications must be kept
HIV classification
ELISA test
(Conner, Fan & Villarreal, 2007)
(Conner, Fan & Villarreal, 2007)
HIV Budding
Clinical manifestations of HIV/AIDS
(Conner, Fan & Villarreal, 2007)
(bodypro, 2003)
HIV destroys crucial CD4+ cells
(WHO, 2011)
(Judd, 2011)
(Judd, 2011)
(Sciencephotolibrary, n.d.)
(dnatube, 2007)
(Judd, 2011)
Aids.gov. (2012). [Image]. What is HIV/AIDS? Retrieved from: http://aids.gov/hiv-aids-basics/hiv-aids-101/what-is-hiv-aids/

Anderson, D. G., Nester, E. W., Roberts, C. E. (2012). HIV disease and complications of immunodeficiency. In microbiology: a human perspective, seventh edition (pp. 694-715). New York, NY. McGraw-Hill.

Bodypro. (2003). [Image]. Beta chemokines block entry into the cell. Retrieved from: http://www.thebodypro.com/content/art4978.html

Conner, R.F., Fan, H. & Villarreal, L.P. (2007). AIDS Science and Society: fifth edition. New York, NY: Jones & Bartlett Learning.

Connexions. (2013). [Image]. Stem cells. Retrieved from: http://cnx.org/content/m46036/latest/?collection=col11496/latest

Cosmos. (2013). [Image]. HIV virus. Retrieved from: http://www.cosmosmagazine.com/news/theory-how-hiv-attacks-wrong/

Dnatube. (2007). HIV lifecycle. [Video file]. Retrieved from:

Judd, Sandra. (2011). AIDS sourcebook: fifth edition. Retrieved from: Gale virtual reference library.

Kuitkuppala Surya Rao, P. (2009). CCR5 inhibitors: Emerging promising HIV therapeutic strategy. Department of Family Medicine, Kutikuppala Suryarao Hospital. Vol. 30, No. 1, pg. 1-10.

Merck Manual of medical information. (2012). New york, NY. Pocket books.

Moore, P. (2007). The little book of pandemics. New York, NY. HarperCollins.

Physicians research network. (2013). [Image]. Understanding pathogenesis. Retrieved from: http://www.prn.org/index.php/progression/article/hiv_pathogenesis_57

Science photo library. (n.d.). [Image]. Colored TEM of HIV viruses, that causes AIDS. Retrieved from: http://www.sciencephoto.com/media/248367/view

Shabb, S. (2013). Biotech breakthroughs seminar. Highline Community College.

Turbosquid. (2013). [Image]. Human brain. Retrieved from http://www.turbosquid.com/3d-models/3d-brain-human-man/564818

World Health Organization. (2011). [Image]. Global health observatory map gallery. Retrieved from: http://gamapserver.who.int/mapLibrary/app/searchResults.aspx

References (Continued):
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