Oncogenic and Retroviruses 2021

@David lufafa
Oncogenic and Retroviruses
Dr. Kabanda T
ID Consultant
7/21/2021 Oncogenic and Retro-Viruses

Oncogenic viruses
• Cancers are the result of a disruption of the normal restraints
on cellular proliferation.
• There are two classes of these genes in which altered
expression can lead to loss of growth control
• Those genes that are stimulatory for growth and which cause
cancer when hyperactive. Mutations in these genes will be
dominant. These genes are called oncogenes.
• Those genes that inhibit cell growth and which cause cancer
when they are turned off. Mutations in these genes will be
recessive. These are the anti-oncogenes or tumor-suppressor
genes.
•
What do oncogenes encode?
Proteins that are involved

in growth control and
differentiation:
Growth factors
Growth factor receptors
Signal transduction proteins
Transcription factors

The 2 major concepts of the way viral
tumorigenesis
• The provirus modes.
• The oncogene model. The genes for malignancy are

already present in all cells. These oncogenes encode proteins that
encourage cell growth, eg, fibroblast growth factor, Signal
transduction proteins etc. In this model, carcinogens such as
chemicals, radiation, and tumor viruses activate cellular
oncogenes to overproduce these growth factors. This initiates
inappropriate cell growth and malignant transformation.

Oncogenic viruses
• Viruses are involved in cancers because they can
either carry a copy of one of these genes or can alter
expression of the cell's copy of one of these genes.
• If a virus takes up residence in a cell and alters the
properties of that cell, the cell is said to be
transformed
• Transformation often includes loss of growth control,
ability to invade extracellular matrix and de-
differentiation.
• In carcinomas, many epithelial cells undergo an
epithelial-mesenchymal
7/21/2021
transformation. Transformed
Oncogenic and Retro-Viruses
Retroviral oncogenes
Avian Myeloblastosis Virus
R U5 GAG POL MYB U3 R
Feline Sarcoma Virus (FSV)
R U5 dGAG FMS dENV U3 R
Avian Myelocytoma Virus (MC29)
R
7/21/2021
U5 dGAG MYC dENV
U3 R
Some retroviruses have an
extra gene
“typical retrovirus”
R U5 GAG POL ENV U3 R
Rous Sarcoma Virus
R U5 GAG POL ENV SRC U3 R

CLASSES OF TUMOR VIRUSES
• There are two classes of tumor viruses:

• A. DNA tumor viruses
• B. RNA tumor viruses, also referred to as
RETROVIRUSES

Human cancer viruses
• Viruses are etiologic factors in the development
of several types of human tumors, including two
of great significance worldwide—cervical cancer
and liver cancer.
• At least 15–20% of all human tumors worldwide
have a viral cause.
• RNA tumor viruses involve cellular oncogenes in
neoplasia
• DNA tumor viruses establish a role for cellular
tumor suppressor genes.
Oncogenic viruses
DNA viruses RNA viruses
– Herpesvirus – Retrovirus
– Adenovirus – Flavivirus
– Hepadnavirus
– Papillomavirus
– Poliomavirus
– Poxvirus

Viruses strongly associated with human
cancers

RNA TUMOR VIRUSES
(RETROVIRUSES)
• RNA genome
• integrated into host genome.
• Since RNA makes up the genome of the mature virus
particle, it must be copied to DNA prior to
integration into the host cell chromosome.
• This life style goes against the central dogma of
molecular biology in which DNA is copied into RNA.
• Include: Oncovirinae, Spumavirinae and Lentivirinae

Not all tumor viruses of the retrovirus
family contain onc genes.
How do these viruses cause malignant
transformation?
The DNA copy of the viral RNA integrates near a

cellular oncogene, causing a marked increase in its
expression.
Overexpression of the cellular oncogene may play
a key role in malignant transformation by these
viruses.

ONCOVIRINAE
• The first member of this group to be discovered was
Rous Sarcoma Virus (RSV) - which causes a slow
neoplasm in chickens.
• Viruses in this group that cause tumors in humans
are:
• HTLV-1 (human T-cell lymphotropic virus-1) which
causes Adult T-cell Leukemia (Sezary T-cell
Leukemia). HTLV-1 is sexually transmitted
• HTLV-2 (human T-cell lymphotropic virus-2) which
causes Hairy Cell Leukemia. This virus is endemic to
very specific regions
7/21/2021
of the Americas, particularly in
SPUMAVIRINAE
• Cells infected by spumaviruses have a foamy
appearance (because of numerous vacuoles) and
often form syncytia of giant multinucleate cells.
• They have been isolated from primates (including
humans), cattle, cats, hamsters, and sea lions
• Chimpanzee (simian) foamy virus is the type species.
• Human foamy virus is a variant of simian foamy virus
and is usually acquired from a monkey bite.
• There is no evidence of pathological effects of these
viruses.
LENTIVIRINAE (SLOWVIRUSES)
• These have a long latent period of infection

before disease occurs;
• Includes HIV (formerly HTLV-III) which causes
AIDS.
• It is much more closely related to some
Lentivirinae than it is to HTLV-I and HTLV-II

Retroviruses
❖Baltimore and Temin class vi
❖RNA-dependent DNA polymerase (reverse
transcriptase ) encoded by retroviruses
❖Retroviruses replicate through an DNA intermediate
❖This DNA copy of viral genome integrates into host
chromosome
❖This discovery earned the Nobel prize: contradicted
the central dogma of molecular biology-genetic
information passed from DNA to RNA and then to
protein
❖Here: from RNA to DNA
History
• 1981: first human retrovirus: Human T-

lymphotropic virus (HTLV-1)
• 1983: Human immunodeficiency virus
(HIV)

retroviruses
HIV and AIDS

HIV
• Is a retrovirus that
belongs to the lentivirus
family
• The virus targets mainly
CD4+ cells
• Target cells include T
lymphocytes, Dendritic
cells and Macrophages
• Causes Acquired
Immune deficiency
Syndrome (secondary)
HIV introduction
• There are two types of HIV: HIV-1 and HIV-2.
• Clinically indistinguishable disease, the time to
disease onset is longer for HIV-2.
• The worldwide epidemic of HIV and AIDS is
caused by HIV-1 while HIV-2 is mostly
restricted to west Africa
• HIV-2 shares 40% nucleotide homology with
HIV-1

Structure of HIV
gp 120
gp 41
Matrix proteins
Envelope
Nucleocapsid with
RNA and enzymes

HIV structure
• Is an RNA virus
• Contains two identical
copies of positive sense
RNA genome (Diploid)
• Contains three typical
retroviral genes gag, pol
and env which code for
structural proteins
• Regulatory genes tat, rev
required for replication
• Accessory genes nef, vif, vpr
and vpu not required for
replication

Surface structures
• The outer envelope comes from
the host cell plasma membrane
• Coat proteins (surface antigens)

are encoded by env (envelope)
gene and are glycosylated.
• One primary gene product (gp
160) is made but this is cleaved
to gp 120 and gp41 (cleavage is
by host enzyme protease.
• gp 120 is for attachment
• gp41 is for fusion with host cell

Internal structure
gag coded proteins
• P17 matrix (MA) protein lines the inner
surface of viral membrane and P24
(nucleocapsid protein protects the viral
genome). These are cleaved by a virally-
coded protease
pol coded proteins

• Reverse transcriptase - copies RNA
genome into double stranded DNA
• Integrase - integrates the double stranded
DNA into the host cell chromosome
• Protease - cleaves the pol and gag-
encoded polyproteins
Viral genome
diploid RNA

The Genome of HIV

TYPING OF HIV
• Two types of HIV, HIV 1 and 2, 40% homology
• HIV-1 is the cause of the worldwide AIDS pandemic
• HIV-2 is found in west Africa but rarely elsewhere

.
• HIV-2 causes AIDS much more slowly than HIV-1
• Both HIV-1 and HIV-2 are thought to have arisen from simian
immunodeficiency virus (SIV)
• HIV-2 is closely related to the SIV found in west Africa.

HIV subgroups/genotypes
• There are three sub-groups
of HIV-1, M (main or major),
N (new) and O (outlier).
• Type O HIV-1 is mostly
found in Cameroon and
Gabon while the rare N sub-
group is also found in
Cameroon.
• It is thought that SIV
infected humans on
separate occasions to give
rise to the three sub-
groups.

HIV subtypes
• Aleast ten different HIV-1
subtypes(clades) within the M
group - these are designated A to
J.
• The major one in North America,
Latin America and the Caribbean,
Europe, Japan and Australia is
type B.
• Most sub-types are found in sub-
Saharan Africa with A and D
found at the highest rates in
central and eastern Africa and C
in southern Africa.

HIV subtypes/clades
• Type C is also the predominant
form in India and Nepal. It is type
C that has caused the most
infections worldwide.
• Type E is found in Thailand and
central Africa,
• type F in Brazil and Romania, type
G in Russia and Gabon, while type
H is found in Zaire and in
Cameroon. Subtype K is found in
the Congo and Cameroon.
Subtype I was a name given to an
apparent sub-type found in
Cyprus but the name is no longer
used.

HIV subtypes and transmission
dynamics
• Different HIV-1 subtypes can be transmitted by different
routes.
• For example, type B found in western countries, may be
transmitted more effectively by homosexual intercourse and
via blood (as in intra-venous drug use)
• Types C and E may be transmitted more via a heterosexual
route. This is because types C and E replicate better in
Langerhans' cells found in the mucosa of the cervix, vagina
and penis while type B replicates better in the rectal mucosa.
• It also appears that type E is more readily transmitted
between sexual partners than type B.
• Subtype D seems to be more virulent than subtype A
• In addition subtypes D and C seem to be transmitted more
effectively from mother to child than subtype A.
HIV replication

The Replication of HIV

Viral replication
• 1. Binding of the virion to CD4 receptor
using gp120 and interaction with co-
receptors CxCR4 and CCR5. The T cell
Tropic strains bind to CXCR4 whereas the
macrophage tropic strains bind to CCR5
• 2) Uptake by direct fusion to the plasma

membrane. This requires expression of
Co-receptors and gp41
• 3) RNA (plus sense) is copied by reverse

transcriptase to minus sense DNA. Here,
the polymerase is acting as an RNA-
dependent DNA polymerase. Since
reverse transcriptase is a DNA
polymerase, it needs a primer. This is a
tRNA that is incorporated into the virus
particle from the previous host cell.

Replication of HIV
• 4) RNA is displaced and degraded by a
virus-encoded RNase H activity. Reverse
transcriptase now acts as a DNA-
dependent DNA polymerase and copies
the new DNA into a double strand DNA.
This DNA form of the virus is known as a
the provirus.
• 5) Double strand DNA is circularized and

integrated into host cell DNA using a
virally encoded integrase enzyme. This
DNA is copied every time cellular DNA is
copied. Thus, at this stage the provirus is
just like a normal cellular gene.
• 6) Full length, genomic RNA (plus sense) is

copied from the integrated DNA by host
RNA polymerase II which normally copies
a gene to mRNA. The genomic RNA is
capped and poly adenylated, just as an
mRNA would be.

Viral replication
• 7.Since the full length genomic
RNA is the same sense as
message, it also acts as the mRNA
for GAG and POL polyproteins.
• 8.The genomic RNA is spliced by
host nuclear enzymes to give
mRNA.
• mRNA is translated into several
polyproteins.
• The Gag and Pol polyproteins are
cleaved by the viral protease
while the EnV polyprotein is
cleaved by cellular protease

Epidemiology of HIV/AIDS

HIV in numbers
• World wide pandemic
• 33M infected, 22M in
sub-Saharan
• 14000 new infection
daily
• 3M death/yr, 25M
overall
• Ug prevalence 7.3%

Transmission of HIV
• By sexual contact (57%)

• By transfer of infected blood (13%)
• By injection (13%)
• Vertical transmission - from infected
mother to neonate, either at birth or via
breast milk (17%)

Risk factors for HIV transmission
• Multiple concurrent sexual partners
• STD especially the ulcerative types like syphilis
and chancroid
• MSM especially receptive anal intercourse
• Blood transfusion especially if inadequately
screened (Window period)
• Occupational exposure in health workers

Pathogenesis and clinical features of HIV
• HIV progresses in 3 stages

– Acute retroviral syndrome
– Latent HIV
– Overt AIDs

Acute infection (acute retroviral syndrome
• If acquired by sexual activity, the virus enters the

body through infected macrophages in semen or
vaginal secretions.
• Dendritic cells in the mucosal linings bind the virus
shed by macrophages and carry it to the lymph
nodes where CD4+ T4 cells become infected.
• During the course of the disease, the virus migrates
to other cell types.

Acute infection ctd
• Initially, HIV infection
produces a mild disease
that is self-limiting.
• This is not seen in all
patients and about half
remain asymptomatic
during the initial period of
infection.
• In the period immediately
after infection, virus titer
rises (about 4 to 11 days
after infection) and
continues at a high level
over a period of a few
weeks

Acute infection
• 4). The patient often experiences
some mononucleosis-like
symptoms (fever, rash, swollen
lymph glands) but none of these
is life-threatening.
• There is an initial fall in the
number of CD4+ cells and a rise in
CD8+ cells but they quickly return
to near normal.
• At this stage virus titers are very
high with as many as one
hundred million virus particles
per milliliter of plasma

Acute HIV infection ctd
• There is a "window period" of
seronegativity during which an
infected person does not give a
positive western blot HIV test or
ELISA,
• The viral load is high and the
patient may exhibit some
symptoms.
• This seronegative period can last
for six months before
seroconversion although the
latter usually occurs between one
and four weeks after infection.

Copyrights apply

Acute HIV infection ctd
• T lymphocytes mount an antiviral defense and virus largely

disappears from the circulation.
• After the increased cell-mediated immune response, there is
a rise in humoral antibodies.
• During this period of strong immune response to the virus,
more than 10 billion new HIV particles are produced each day
but they are rapidly cleared by the immune system and have a
half life of only 5 to 6 hours (some estimates show a half life
of minutes).
• At this stage, most of this virus is coming from recently
infected proliferating CD4+ cells

Acute HIV syndrome
• The infected cells that are producing this virus are destroyed
either by the immune system or by the virus and have a half
life about 1 day.
• However, the rate of production of CD4+ cells can compensate
for the loss of cells and a steady state is set up in which most
CD4 cells are uninfected.
• After infection, activated T cells are destroyed by the immune
system, but a small fraction of the productively infected cells
may survive long enough to revert back to the resting memory
state (as do none-infected CD4+ memory cells).
• The resting memory cells do not express viral antigens but do
carry a copy of the HIV genome which remains latent until the
cells are reactivated by antigen
• During this period, the virus disseminates to other regions
including to lymphoid and nervous tissue. This is the most
infectious phase of theOncogenic
7/21/2021 disease .
and Retro-Viruses
Latent HIV
• As a result of the strong immune defense, the number of viral
particles in the blood stream declines and the patient enters
clinical latency.
• Little virus can now be found in the bloodstream or in

peripheral blood lymphocytes and, initially, the number of
blood CD4+ cells is only slightly decreased.
• Nevertheless, the virus persists elsewhere, particularly in

lymph nodes and here viral replication continues as follicular
dendritic cells interact with more CD4 cells that become
infected.
•7/21/2021
The virus is also replicated by
Oncogenic andmacrophages.
Retro-Viruses
Incubation
• Adults with no treatment: 8-

10years
• ‘rapid progressors’ : 2-3 years
• ‘non-progressor’ : 7-10 years

Stable CD4 cell count
Loss of CD4+ cells and abortion of the
immune response (mechanisms of CD4
cell loss)
• During the course of infection, there is a profound loss of the
specific immune response to HIV because:
• responding CD4+ cells become infected. Thus, there is clonal
deletion leading to tolerance. The cells that proliferate to
respond to the virus are infected and killed by it
• Epitope variation, can lead to escape of HIV from the immune
response
• Activated T cells are susceptible to apoptosis. Spontaneous
apoptosis of uninfected CD4+ and CD8+ T cells occurs in HIV-
infected patients. Also there appears to be specific apoptosis
of HIV-specific CD8+ cells
• the number of follicular dendritic cells falls over time,
resulting in diminished capacity to stimulate CD4+ cells
• Sycytial formation
• Retroendotherial hypoplesia (BM suppression)

Onset of disease - AIDS
• The period of clinical latency varies in length from as little as 1

to 2 years to more than 15 years (Av 8-10).
• Onset of AIDS is rare in less than 3 years except in children.
• The virus can no longer be controlled as helper CD4+ (T4) cells
are destroyed.
• The killer cells needed to control HIV also damage the helper
T cells that they need to function efficiently.
• With the lack of CD4+ cells, new cytotoxic T cell responses
cannot occur as helper cells are lacking and such new
responses are required as the virus mutates.
• As the CD4 cells fall below 200, virus titers rise rapidly and
immune activity drops precipitously.
• It is the loss of immune competence that enables normally
benign opportunistic parasites such as viruses, fungi or
protozoa to cause infections

Opportunistic Infections
Protozoal toxoplasmosis, crytosporidosis, isospora, strongyloides
Fungal candidiasis, crytococcosis, pneumocystitis

histoplasmosis, coccidiodomycosis
Bacterial Mycobacterium avium complex, MTB

atypical mycobacterial disease
salmonella septicaemia
multiple or recurrent pyogenic bacterial infection
Viral CMV, HSV, VZV, JCV

Common opportunistic infections
in AIDS patients
Site of infection L Disease or symptom Causative organism
Lung Pneumonia Pneumocystis, CMV
Mycobacterium
TB tuberculosis
Mouth Thrush Candida

Hairly leucoplakia EBV
Ulceration HSV-1,Hisstoplasma
capsulatum
Esophagus Thrush Candida Albicans

Esophagitis CMV, HSV-1
Intestinal tract Diarrhoea Salmonella spp, shigella,

CMV, Cryptosporidium,
Isospora, Giardia lamblia,
strongyloides stercolaris

Common opportunistic infections
in AIDS patients
Site of infection L Disease or symptom Causative organism
CNS Meningitis Cryptococcus neoformans

EBV
CNS lymphoma JC virus
Progress multifocal
leukoencephalopathy
(PML)
Eye Retinitis Cytomegalovirus
Skin KS and Castleman’s Human Herpes virus-8

disease Varicella zoster virus
HZ Cryptococcus neoformans
Subcutaneous nodules
Reticuloendothelial LN or splenomegally, Mycobacterium avium
system Lymphoid interstitial complex
pneumonitis (LIP) EBV
Copyrights apply
Laboratory diagnosis

Lab diagnosis of HIV
Copyrights apply

Laboratory diagnosis
• Serology: Adults and children older than 15
months:
• Initial screening: ELISA, latex agglutination
• Confirmation: Western-blot
• Molecular techniques:
-qualitative DNA detection: babies younger
than 15 months
-quantitative RNA: follow up of HIV
infected people who are on therapy

Copyrights apply
Copyrights apply
Other diagnostic assays
• It normally takes 4-6 weeks before HIV-antibody appears

following exposure.
• A diagnosis of HIV infection can be made earlier by the
detection of HIV antigen (P24, P17) , proviral-DNA, and
RNA.
• Viral load testing is used to monitor treatment and
emergency of resistance

Treatment of HIV
http://en.wikipedia.org/wiki/HIV

Treatment
• Requires a combination of drugs (HAART)
• Drugs are designed to interfere with the viral replication cycle
• Classes of drugs include-
➢ Entry inhibitors
➢ Reverse transcriptase inhibitors
➢ Intergrase inhibitors
➢ Protease inhibitors
➢ Fusion Inhibitors

Antiretroviral Drugs
• Reverse transcriptase (RT) inhibitors interfere with reverse
transcription. There are two main types of RT inhibitors.
• Nucleoside/nucleotide RT inhibitors are faulty DNA building

blocks and lead to chain. Include Zidovudine, lamivudine,
Abacavir, zalcitabine, Tenofovir
• Non-nucleoside RT inhibitors bind to RT, interfering with its

ability to convert the HIV RNA into HIV DNA. e.g Efavirenz,
Nevirapine, Diltegravir

Antiretroviral Drugs
• Protease inhibitors interfere with the protease
enzyme that HIV uses to produce infectious viral
particles. Include Saquinavir, Lopinavir, Indinavir.
• Entry and fusion inhibitors interfere with the virus'

ability to fuse with the cellular membrane, thereby
blocking entry into the host cell. e.g Enfuvirtude.
• Integrase inhibitors block intergrase, the enzyme

HIV uses to integrate genetic material of the virus
into its target host cell. E.g Raltegravir
• Treatment is life long and not CURATIVE but it is
preventive
Prevention
• A,B,C,C,D
• PEP/PrEP
• Compliancy to HAART in HIV positive patients
• Treatment of STI
• Screening of blood before use
• Single use of sharps,
• Sterilization of instruments for surgery, acupuncture,
body piercing
• Avoid sharing objects that can easily be
contaminated e.g toothbrushes
• Prevention of maternal to child transmission (PMTC)
Prevention and control
10% household bleach(% 0.5 chlorine,
5g/litre
5000ppm
70% ethanol
2% glutaraldehyde
4% formaldehyde
6% Hydrogen peroxide
Washing laundry in hot water with detergent is
sufficient to inactivate HIV.
Male circumcision reduces
transmission of HIV
• Decreased female to male transmission in men who
are circumcised.
– Male circumcision also reduced acquisition of Herpes
simplex virus and Human papilloma virus, but not syphilis
in study in Uganda (Tobian AAR et al. male circumcision for the prevention of HSV-2 and
HPV infections and syphilis. NEJM 2009 Mar 26; 360:1298)
– Trial of circumcision for HIV pos men with HIV neg women
partners in Uganda did NOT show benefit of circumcision.
(Wawer MJ et al. Circumcision in HIV-infected men and its effect on HIV transmission to female
partners in Rakai, Uganda: A randomized controlled trial. Lancet 2009 Jul 18; 374:229).

The Almighty
Pardons and Grants me heaven

Even if I don't know a single letter about
Crutz Feld Jacob’s Disease
Tsutsugamushi Fever
Criggler Najjar Syndrome
South American equine encephalitis and
Many and much more rarer topics
BUT …….

The Almighty
Will drag me to hell and will not pardon

My ignorance of even the minute details of HIV
My indifference to apply the current knowledge
My negligence in screening for Opportunistic
infections
My despondency about preventing Drug
resistance
My inadequacy in maintaining my patients
as virally suppressed as humanly possible–
7/21/2021 (This is applicable to all
Oncogenic common diseases)
and Retro-Viruses
THE END
Occam’s Razor
May Not Apply

Oncogenic and Retroviruses 2021

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Oncogenic and Retroviruses 2021

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@David lufafa

Oncogenic and Retroviruses

7/21/2021 Oncogenic and Retro-Viruses

Proteins that are involved

7/21/2021 Oncogenic and Retro-Viruses

• The provirus modes.

• The oncogene model. The genes for malignancy are

7/21/2021 Oncogenic and Retro-Viruses

Avian Myeloblastosis Virus

R U5 GAG POL MYB U3 R

Feline Sarcoma Virus (FSV)

R U5 dGAG FMS dENV U3 R

Avian Myelocytoma Virus (MC29)

R U5 GAG POL ENV U3 R

Rous Sarcoma Virus

R U5 GAG POL ENV SRC U3 R

7/21/2021 Oncogenic and Retro-Viruses

• There are two classes of tumor viruses:

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

The DNA copy of the viral RNA integrates near a

7/21/2021 Oncogenic and Retro-Viruses

• These have a long latent period of infection

7/21/2021 Oncogenic and Retro-Viruses

• 1981: first human retrovirus: Human T-

7/21/2021 Oncogenic and Retro-Viruses

HIV and AIDS

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

• Coat proteins (surface antigens)

7/21/2021 Oncogenic and Retro-Viruses

pol coded proteins

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

• Two types of HIV, HIV 1 and 2, 40% homology

• HIV-1 is the cause of the worldwide AIDS pandemic

• HIV-2 is found in west Africa but rarely elsewhere

• HIV-2 is closely related to the SIV found in west Africa.

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

• 2) Uptake by direct fusion to the plasma

• 3) RNA (plus sense) is copied by reverse

7/21/2021 Oncogenic and Retro-Viruses

• 5) Double strand DNA is circularized and

• 6) Full length, genomic RNA (plus sense) is

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

• By sexual contact (57%)

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses

• HIV progresses in 3 stages

7/21/2021 Oncogenic and Retro-Viruses

• If acquired by sexual activity, the virus enters the

7/21/2021 Oncogenic and Retro-Viruses

7/21/2021 Oncogenic and Retro-Viruses