1. HUMAN IMMUNEDEFICIENCY VIRUS (HIV)
RETROVIRUSES
HUMAN IMMUNEDEFICIENCY VIRUS (HIV)

2. Teaching objectives State the routes of HIV transmission
Describe HIV pathogenesis
List the clinical features of HIV infection
Describe disease staging and AIDS-defining illnesses
Describe how clinical features and serology are used in diagnosis
Outline how HIV is treated and prevented

3. RETROVIRUSES The Family is divided into three sub families:
Oncovirinae - oncogenic virus- cause sarcomas and leukaemia in human and animals; Lentivirinae - slow progressive degenerative disorders eg HIV 1 & 2
Spumavirinae - no pathology known

4. HUMAN IMMUNEDEFICIENCY VIRUS (HIV)
Causes Acquired Immunedeficiency Syndrome (AIDS)
HIV-1 and HIV-2
HIV-1 is found world wide and is more virulent
HIV-2 is found in West Africa and is less virulent

5. MORPHOLOGY
It is icosahedral in shape
Outer envelope studded with spikes formed by envelope (gp120) and transmembrane (gp41) glycoproteins
Central core contains
viral proteins (gp24)
RNA genome
enzymes

6. Morphology of HIV

7. Source: https://aidsinfo. nih

8. Virus Stability
HIV is inactivated by Heat (autoclave, hot air oven) Glutaraldehyde 2% Hypochlorite (domestic bleach) 70% Alcohol e.g Spirit.
HIV survive
up to 15 days at room temperature
at 37oC – 15 days
over 60oC inactivated 100 – fold each hour

9. HIV GENOME Consists of two identical molecules of single stranded RNA
Have 3 genes
the gag (group-specific antigen) gene
the pol (polymerase) gene
the env (envelope) gene
the genome has other five genes several of which are regulatory genes

10. The gag gene encodes internal core proteins,
the most important of which is p24 an antigen used in serologic test
The pol gene encodes several proteins including:
Reverse transcriptase – synthesize DNA from RNA
Intergrase – Intergrates viral DNA into host DNA
Protease – Cleaves the various viral precursor proteins

11. The env gene encodes gp 160 a precursor glycoprotein
is cleaved by proteases to form the two envelope
proteins gp120
and gp41

12. Transmission of HIV
Sexual contact: HIV is present in semen and vaginal secretions; either homoxesual or heterosexual contact
Transfusions: whole blood, plasma, clotting factors or cellular fractions of blood.
Contaminated needles&sharps: accidentally or sharing needles by drug users.
Perinatal: Transplacenta, during delivery or via breast milk

13. HIV life cycle There are seven stages of the HIV life cycle
1) Attachment: HIV binds (attaches)
to the receptors on the surface of a CD4 cell with the help of co receptor i.e CCR5 and CXCR4
2) Fusion :The HIV envelop and the CD4 cell membrane fuse which allow HIV to enter the CD 4 cell
3) Reverse transcription: inside the CD4 releases and uses reverse transcriptase (an HIV enzyme) to convert its genetic material HIV RNA to HIV DNA allowing HIV to enter CD4 cell nucleus and combine with the cell genetic material cell DNA

14. Newly formed immature HIV pushes itself out of the CD4 cell
4) Integration: Inside the CD4 cell nucleus HIV releases Integrase ( an HIV enzymes).HIV uses integrase to insert its viral DNA into the DNA of the CD4 cell.
5) Replication: HIV releases protease which breaks the long protein chains that form the immature virus
6) Assembly: HIV Proteins and HIV RNA move to the surface of the cell and assemble into immature ( non infectious HIV)
7) Budding:
Newly formed immature HIV pushes itself out of the CD4 cell

15. HIV life cycle: Source:(Prokofjeva et al 2016)
. 2016)

16. Pathogenesis
The cell receptor for HIV-1 is CD4 molecule found on several cell types, helper T cells,macrophages, and dendritic cells Successful infection requires further interaction of the virus with co- receptors on the CD4 cells, these are the chemokine receptors CCR5 and CXCR4 or fusin

17. Attachment of the virion occurs when a site on gp120 recognizes a site on the outer domain of CD4. The interaction of gp120 with the receptor and co-receptor results in a dramatic re-arrangement of gp41, which proceeds to fuse the membranes of the virion and the cell.

18. The contents of the virion are released into the cytoplasm,
the capsid is removed to release the viral genome
Then the virion RNA dependent DNA polymerase transcribes the genome RNA into dsDNA
The virion Intergrase then integrate the dsDNA into the host cell DNA

19. The host cell RNA polymerase transcribes the proviral DNA into mRNA and Viral RNA
The formed mRNA is then translated into several large viral polyproteins

20. The viral polyproteins are then cleaved by the virus encoded Protease to form the viral reverse transcriptase, the core proteins, and the two envelope glycoprotein
i.e. gp120 and gp41
Then the virion assemble on the Plasma membrane of the infected cell and they are released by budding

21. The T4 cell plays a central role in all aspects of immune system function,
death or impairment of this cell results in widespread immune dysfunction
Infection of these cells by the virus and replication of the virus in these cells, leads to the destruction of the infected cells

22. CLINICAL SIGNS HIV infection progresses through three Phases
Acute Retroviral Syndrome
During this phase, a person may experience non-specific ‘flu-like’ symptoms
They do not lead directly to the diagnosis of HIV infection and may not be present in all patients, but commonly include:
Fever, lymphadenopathy, sore throat, mucocutaneous lesions, myalgia/arthralgia, diarrhoea, headache, nausea/vomiting, and weight loss.

23. High turnover of CD4 cells
Clinical Latent Phase
During the latent phase, a person has no symptoms or signs of HIV, and:
High turnover of CD4 cells
Continuous destruction and compensatory increased production of CD4 lymphocytes
Viral reservoir and resting infected cells, which are in the lymph nodes, brain, and testes
even during the latent phase, viral replication and CD4 destruction are occurring, along with gradual destruction of the lymph node. This process is not entirely stable; rather, the destruction of CD4 cells occurs slowly but progressively exceeds the body’s ability to replenish them.
During the period of asymptomatic infection, patients generally have no findings on physical examination except for possible lymphadenopathy.
"Persistent generalized lymphadenopathy" (PGL) is defined as enlarged lymph nodes involving at least two noncontiguous sites other than inguinal nodes.
There is a high rate of HIV replication and destruction during the latent period. Cell death and replacement are in near balance during this phase of the illness and viral load remains stable. The latent phase is also known as the asymptomatic phase.
The current drugs used do not reach the reservoirs. Also, because the viruses are hiding and not active, the drugs are unable act.
that another term for this phase is no significant immunodeficiency.

24. Early Symptomatic Phase or mild immunodeficiency.
Presentation depends on CD4 count
At CD4 cell counts over 500 cells/µl, PLHIV may develop complications in diseases found in the general population:
Malaria
Bacterial pneumonia
Tuberculosis
Minor s
Skin conditions
At CD4 counts between 200 and 500 cells/µl, other conditions, or opportunistic infections, begin to appear:
Pulmonary Tuberculosis
Oral or vaginal candidiasis
Herpes zoster
although PLHIV may develop complications found in the general population, they may experience these complications more frequently than would someone with a healthier immune system.
another term for this phase is mild immunodeficiency.

25. Late Symptomatic Phase or advanced immunodeficiency.
The late symptomatic phase is characterized by patients having a CD4 cell count less than 200 cells/µl and conditions such as:
Wasting syndrome
Oesophageal candidiasis
Atypical and extra-pulmonary TB
Pneumocystis pneumonia
Recurrent invasive herpes simplex virus infections
approximately 10% of patients develop an AIDS-defining diagnosis even when their CD4 count is above 200/mm3.
atypical and extra-pulmonary TB further. According to WHO staging book, they mean “Disseminated non-tuberculous mycobacterial infection and Extrapulmonary tuberculosis.”
another term for this phase is advanced immunodeficiency.

26. Severe HIV Infection and AIDS
This phase is characterized by patients having a CD4 cell count less than 50 cells/µl and conditions such as:
Cryptococcus meningitis
Cryptosporidiosis
Toxoplasmosis of the brain
HIV encephalopathy (dementia)
CMV retinitis
another term for this phase is severe immunodeficiency.

27. AIDS Manifestations: Children
Advanced HIV infection and AIDS manifest differently in children
Common manifestations include:
Diarrhoea
Pulmonary conditions
Malnutrition and failure to thrive
Central nervous system problems
Dermatitis
Otitis media
Kaposi sarcoma
Parotid enlargement
Cardiac, renal problems
pulmonary conditions may include TB, PCP, bacterial pneumonia, or LIP.
LIP is lymphocytic interstitial pneumonia, a disease secondary to autoimmune disorders such as HIV.
Symptoms include fever, cough, and shortness of breath and patients may present with lymphadenopathy, enlarged liver, enlarged spleen, enlarged salivary gland, thickening and widening of the extremities of the fingers and toes, and breathing symptoms such as shortness or breath and wheezing.
EXPLAIN to participants that central nervous system problems in children can include: HIV encephalopathy, neuropathy, seizures, CMV, Cryptococcus, and Toxoplasmosis.
EXPLAIN to participants that dermatological issues can include: central seborrhoea, atopic, eczema, and psoriasis.

28. WHO staging system for HIV infection and disease in adults (1)
WHO identified 4 clinical stages based on the performance level of the person and the associated illnesses:
Clinical stage I
Asymptomatic
Generalised lymphadenopathy
Performance Scale 1: asymptomatic, normal activity
Clinical Stage II
Weight loss <10% of body weight
Minor mucocutaneous manifestations (seborrhoeic dermatitis, prurigo, fungal nail infections, recurrent oral ulcerations, angular cheilitis)
Herpes zoster within the last 5 years
Recurrent upper respiratory tract infections (e.g., bacterial sinusitis)
And/or Performance Scale 2: symptomatic, normal activity

29. Clinical stage III Weight loss >10% of body weight
Unexplained chronic diarrhea lasting for more than 1 month
Unexplained prolonged fever (intermittent or constant) lasting for more than 1 month
Oral candidiasis (thrush)
Oral hairy leukoplakia
Pulmonary tuberculosis
Severe bacterial infections (e.g., pneumonia, pyomyositis)
And/or Performance Scale 3: bedridden less than 50% of the day during the past month

30. Clinical stage IV Pneumocystis jiroveci pneumonia
ng syndrome
Pneumocystis jiroveci pneumonia
Toxoplasmosis of the brain
Cryptosporidiosis with diarrhea lasting more than 1 month
Cryptococcus extra-pulmonary
Cytomegalovirus (CMV) disease of an organ other than liver, spleen or lymph node (e.g., retinitis)
Herpes simplex virus (HSV) infection, muco-cutaneous (lasting for more than 1 month), or visceral
Progressive multifocal leukoencephalopathy (PML)
Any disseminated endemic mycosis
Candidiasis of the esophagus, trachea, bronchi
Atypical mycobacteria disseminated or pulmonary
Non-typhoid salmonella septicemia
Extra pulmonary tuberculosis
Lymphoma
Kaposi's sarcoma (KS)
HIV encephalopathy
And/or Performance Scale 4: bedridden more than 50% of the day during the past month

31. Lab Tests Used for HIV Diagnosis
Antibody detection using:
Rapid tests
ELISA
PCR
Assays to detect p24 antigen
Assays to detect HIV DNA or RNA
Viral culture

32. Antibody Tests Effective 12 weeks after infection,
Antibody methods for diagnosing HIV include
Rapid tests
Enzyme Linked Immunosorbent Assay (ELISA)
Western Blot
Effective 12 weeks after infection,
as antibodies appear 6 to 12 weeks following HIV infection in majority of patients
Not suitable for use in infants under 18 months

33. Window Period (1)
HIV antibodies take time to multiply and show up on antibody or antigen tests
The window period
is the period between time of infection and when initial detection of HIV markers is possible by laboratory tests
the window period can last up to six months.
because both Antibody and Antigen tests rely on antibodies, and antibodies take 6-12 weeks to show up on a test, HIV cannot be immediately detected through these tests. For that reason, there is a window period.
this also means that someone can be infected and infectious to others even though the antibody test was negative.

34. Rapid Tests Detect HIV antibodies
Results available in less than 30 minutes
Can use whole blood, plasma, or serum samples
Detection of HIV with rapid test is possible 12 weeks after infection
Not used on infants under 18 months
Rapid Test Algorithm:
Bioline HIV-1/2,
Determine HIV-1/2, Unigold HIV-1

35. National HIV Rapid Test Algorithm
Test 1: Bioline HIV-1/2
Test 2: Determine HIV-1/2
Discordant specimens:
Test 3: Unigold HIV (tie-breaker)
This shows the successive tests that the provider will give in testing a person for HIV. This is further clarified in the next slides.
Capillus is being phased out.

36. National HIV Rapid Test Algorithm
Blood Sample
National HIV Rapid Test Algorithm
Test 1
Bioline
Non-reactive
Result
Report
Negative
Reactive
Result
Test 2
Determine
Reactive
Result
Report
Positive
Non-Reactive
Result
rapid tests give quick results that are available within minutes since:
the test can be done on site and
read by the provider with high diagnostic accuracy that is at least comparable to standard serology
Rapid tests are also cheaper than ELISA.
the roll out of Bioline-based algorithm is being scaled up while the Capillus-based being phased out. Some places still use Capillus, which follow the same algorithm as Bioline.
Test 3 (Tie- breaker)
Uni-Gold
Reactive
Result
Report
Positive
Non-Reactive
Result
Report
Negative

37. Determine: Getting Ready
2. Use 1 strip per test and be sure
to preserve the lot number on the remaining packet of strips
1. Collect test items and other
necessary lab supplies
Images and text adapted from CDC: HIV Rapid Test Training,
Determine is a type of rapid test. The purpose of the next few slides is to provide an example of what rapid testing looks like, and how it works.
The other types of rapid test are Uni-Gold and Bioline (and Capillus, which is being phased out), which follow somewhat similar procedures.
3. Label the test strip with client
identification number
4. Pull off the protective foil cover
Images and text adapted from CDC: HIV Rapid Test Training

38. Determine: Collecting Specimen
Images and text adapted from CDC: HIV Rapid Test Training,
Images and text adapted from CDC: HIV Rapid Test Training
5. Collect 50 µl of specimen using a precision pipette or 1 drop using a plastic transfer pipette

39. Determine: Applying Specimen and Buffer to Test Strip
Images and text adapted from CDC: HIV Rapid Test Training,
7. add 1 drop
of chase buffer to the specimen pad
6. Apply the specimen to the
absorbent pad on the strip
Images and text adapted from CDC: HIV Rapid Test Training

40. Determine: Getting Results
Images and text adapted from CDC: HIV Rapid Test Training,
Images and text adapted from CDC: HIV Rapid Test Training
8. Wait 15 minutes (no longer than 60 minutes) before reading the results
9. Read and record the results
and other pertinent info on the
worksheet

41. Determine: HIV Test Interpretation
Reactive
Non-reactive
A reactive test result means that there are antibodies to HIV in the blood of the person being tested, and the person being tested is HIV-positive.
A non-reactive result means that there are no antibodies to HIV in the blood of the person being tested, and the person being tested is HIV-negative, or is in their window period.
An invalid result means that the control bar did not appear in the control window. A red bar should appear in the control window every time, whether the person is HIV-positive, or HIV-negative. The control bar shows that the test is working, no matter the result. If the control bar does not show up, this means that this test result is not usable, and the test must be repeated.
Images and text adapted from CDC: HIV Rapid Test Training,
Invalid
Images and text adapted from CDC: HIV Rapid Test Training

42. Diagnosis in Children Under 18 Months
HIV diagnosis by serology in infants < 18 months is complicated by presence of maternal antibodies
Diagnosis is by detection of viral nucleic acid material (DNA/RNA) by PCR
If neither virological confirmation nor CD4 is available, start ART in HIV exposed infants <18 months with WHO Paediatric Stage 3 or 4
In such cases, HIV antibody testing must be repeated at age of 18 months to confirm that the child is HIV infected
Only children with confirmed infection should continue ART
an “exposed infant” is an infant born to an HIV-positive mother who is either HIV-positive or else tests positive for HIV because he/she has HIV antibodies from the mother for up to 18 months. An “infected infant” is one who has been confirmed as HIV-infected through a test other than an antibody test.
establishing HIV infection in HIV exposed infants (and children up to 18 months) is difficult for two main reasons:
Maternal HIV antibodies persist for many months
When antiretroviral therapy has been administered to the mother, either as treatment or to prevent mother-to-child transmission, and has also been administered as prophylaxis to the baby, an HIV viral load may be undetectable even in an infected infant
HIV diagnostic efforts should focus on testing pregnant women for HIV
Breastfeeding adds additional risk during infancy period

43. Treatment/Prevention
The medications used are aimed at suppressing one of the key steps of the infection:

44. Entry Inhibitors 
interfere with the virus' ability to bind to receptors on the outer surface of the cell it tries to enter.
When receptor binding fails, HIV cannot infect the cell.
Fusion Inhibitors 
interfere with the virus’s ability to fuse with a cellular membrane, preventing HIV from entering a cell.

45. Reverse Transcriptase Inhibitors
 prevent the HIV enzyme reverse transcriptase (RT) from converting single-stranded HIV RNA into double-stranded HIV DNA―a process called reverse transcription.

46. There are two types of RT inhibitors:
Nucleoside/nucleotide RT inhibitors (NRTIs) are faulty DNA building blocks.
When one of these faulty building blocks is added to a growing HIV DNA chain, no further correct DNA building blocks can be added on, halting HIV DNA synthesis.
Non-nucleoside RT inhibitors (NNRTIs) bind to RT, interfering with its ability to convert HIV RNA into HIV DNA

47. Integrase Inhibitors 
block the HIV enzyme integrase, which the virus uses to integrate its genetic material into the DNA of the cell it has infected.

48. Protease Inhibitors interfere with the HIV enzyme called protease, which normally cuts long chains of HIV proteins into smaller individual proteins.
When protease does not work properly, new virus particles cannot be assembled.
Multi-class Combination Products combine HIV drugs from two or more classes, or types, into a single product.

49. To prevent strains of HIV from becoming resistant to a type of antiretroviral drug, healthcare providers recommend that people infected with HIV take a combination of antiretroviral drugs in an approach called highly active antiretroviral therapy (HAART).
HAART combines drugs from at least two different classes.

50. Anti-HIV drugs approved for use*
Russian name
Latin name
Trade name
FDA approval
Nucleoside reverse transcriptase inhibitor (NRTI)
Zidovudine (1)
Zidovudine (azidothymidine, AZT, ZDV)
Retrovir
19/03/1987
Didanosine (2)
Didanosine (dideoxyinosine, ddI)
09/10/1991
Delayed-release didanosine, enteric-coated didanosine, ddI EC)
Videx EC
31/10/2000
Stavudine (3)
Stavudine (d4T)
Zerit
24/06/1994
Lamivudine (4)
Lamivudine (3TC)
Epivir
17/11/1995
Abacavir (5)
Abacavir (ABC)
Ziagen
17/12/1998
Phosphazide (6)
Azidothymidine H-phosphonate
Nikavir
05/10/1999**

51. Non-nucleoside reverse transcriptase inhibitor (NNRTI)
Nevirapine** (9)
Nevirapine (NVP)
Viramune
21/06/1996
Nevirapine ХR*** (10)
Extended-release nevirapine (NVP XR)
Viramune XR
25/03/2011
Delavirdine (11)
Delavirdine (delavirdine mesylate, DLV)
Rescriptor
04/04/1997
Efavirenz (12)
Efavirenz (EFV)
Sustiva
17/09/1998
Etravirine (13)
Etravirine (ETR)
Intelence
18/01/2008
Rilpivirine (14)
Rilpivirine (RPV)
Edurant
20/05/2011

52. Protease inhibitor (РI)
Saquinavir (15)
Saquinavir (SQV)
Invirase
06/12/1995
Ritonavir (16)
Ritonavir (RTV)
Norvir
01/03/1996
Indinavir (17)
Indinavir (IDV)
Crixivan
13/03/1996
Nelfinavir (18)
Nelfinavir (NFV)
Viracept
14/03/1997
Atazanavir (19)
Atazanavir (ATV)
Reyataz
20/06/2003
Fosamprenavir (20)
Fosamprenavir (FOS-APV, FPV)
Lexiva
20/10/2003
Tipranavir (21)
Tipranavir (TPV)
Aptivus
22/06/2005
Darunavir (22)
Darunavir (DRV)
Prezista
23/06/2006

53. Integrase inhibitor (INI)
Raltegravir (23)
Raltegravir (RAL)
Isentress
12/10/2007
Dolutegravir (24)
Dolutegravir (DTG)
Tivicay
13/08/2013
Elvitegravir (25)
Elvitegravir (EVG)
Vitekta
24/09/2014

54. Drug combinations (cocktails) used in complex treatment of a HIV infection
Trade name
FDA approval
Lamivudine/Zidovudine (3TC/ZDV)
Combivir
27/9/1997
Abacavir/Lamivudine/Zidovudine (ABC/3TC/ZDV)
Trizivir
14/11/2000
Abacavir/Lamivudine (ABC/3TC)
Epzicom
2/8/2004
Emtricitabine/Tenofovir (FTC/TDF)
Truvada
Efavirenz/Emtricitabine/Tenofovir (EFV/FTC/TDF)
Atripla
12/6/2006
Emtricitabine/Rilpivirine/Tenofovir (FTC/RPV/TDF)
Complera
10/8/2011

55. Drug combinations (cocktails) used in complex treatment of a HIV infection
Elvitegravir/Cobicistat/Emtricitabine/Tenofovir (QUAD, EVG/COBI/FTC/TDF)
Stribild
27/8/2012
Abacavir/Dolutegravir/Lamivudine (ABC/DTG/3TC)
Triumeq
22/8/2014
Atazanavir/Cobicistat (ATV/COBI)
Evotaz
29/1/2015
Darunavir/Cobicistat (DRV/COBI)
Prezcobix
Elvitegravir/Cobicistat/Emtricitabine/Tenofovir/Alafenamide (EVG/COBI/FTC/TAF)
Genvoya
5/11/2015

56. The antiviral treatment that is currently used has its limitations.
Patients have to take drugs throughout their lives, while new mutant forms of the virus emerge which are resistant to a wide range of drugs.
Upon long-term therapy, the drugs may cause a cumulative toxic effect.

57. new approach is required to enable the achievement of permanent remission under milder treatment conditions.
Also, life cycle inhibitors suppress HIV-1 only in cells with active viral replication, but they do not affect a latent virus.

58. Viral genome copies integrate into the genome of memory T cells (CD4+ T cells) and remain invisible to the immune system
Induction of transcription in these cells leads to the formation of infectious viral particles

59. The development of an anti-HIV-1 vaccine is an alternative option.
The first vaccine was developed in the early 2000s; however, the effectiveness of vaccination was much lower than that of classic anti- HIV drugs
broad-spectrum neutralizing antibodies is undergoing clinical trials

60. the possibility of affecting a latent virus is being investigated.
the transplantation of bone marrow from donors resistant to the HIV infection (e.g., whose genome contains a mutant gene of HIV-1 co-receptors, Δ32 CCR5).
As shown in 2009, this approach enabled a complete cure of the HIV infection; i.e., all copies of the viral genome were eliminated from the body.
This event was called the “Berlin patient”

61. The patient underwent radiation therapy and bone marrow transplantation from a donor with Δ32 CCR5.
Later, after discontinuation of anti- HIV therapy, the virus could no longer be detected in his body.
But to date, there have been cases where this approach has not had the desired effect. Therefore, the search for other therapies continues.

62. CONTROL SEXUAL TRANSMISSION
Avoid unprotected penetrative sexual intercourse with partners of unknown status
Use condoms
MOTHER TO CHILD TRANSMISSION
Identify infected mothers and give specific therapy in the later stages of pregnancy and to the baby after birth.

63. EXPOSURE TO BLOOD
Drug injectors should stop the practice,
avoid sharing needles or only use sterile
needles.
Screen all blood donors
Screen all organ donors

64. CONTROL cont...
Occupational risk should be minimized by the implementation of safe working practices to prevent accidental injury and contamination with blood and bloody fluids.
e.g. use of gloves, masks and eye protection

65. CONTROL cont... Safe disposal of used needles,
scalpel blades and other sharps
If an accidental exposure occurs
The wound should be washed with soap and water or mucous membrane be flushed with water

66. Assess the risk through knowledge of:
The accident be reported so that prophylaxis can be started
Assess the risk through knowledge of:
The HIV status of the source patient
Is the source on therapy for HIV?

67. Any evidence of resistance?
The nature of exposure, e.g. injury or contamination of the skin or mucous membranes

68. CONTROL cont...
If there is indication of risk, therapy must be started within 1-2 hrs and not later than 48-72hrs
Zidovudine alone can reduce the transmission rate, but should be combined with another RTI e.g. lamivudine and a protease inhibitor
Therapy should be continued for 4 weeks, and the victim be tested for virus after 6 months

69. References
Prokofjeva, M.M., Kochetkov, S.N. & Prassolov, V.S., Therapy of HIV Infection: Current Approaches and Prospects. Acta naturae, 8(4), pp.23–32. Available at:
264 [Accessed January 20, 2017].
The HIV Life Cycle | Understanding HIV/AIDS | AIDSinfo. (n.d.). Retrieved January 20, 2017, from

70. Types of HIV/AIDS Antiretroviral Drugs | NIH: National Institute of Allergy and Infectious Diseases. (n.d.). Retrieved January 20, 2017, from

71. Prevention