Transcript PPT - kimscience.com

The Influenza Virus
• Hemagglutinin
(HA) spikes used
for attachment to
host cells
• Neuraminidase
(NA) spikes used to
release virus from
cell
INFLUENZA ANIMATION
Figure 24.15
The Influenza Virus
• Antigenic shift
– Changes in HA and NA spikes
– Probably due to genetic recombination between
different strains infecting the same cell
• Antigenic drift
– Point mutations in genes encoding HA or NA spikes
– May involve only 1 amino acid
– Allows virus to avoid host cell antibodies
ANTIGENTIC SHIFT ANIMATION
Influenza Serotypes
Type Antigenic Year
Subtype
Severity
Common Name
A
Moderate
Severe
Severe
Moderate
Severe
Low
Spanish Flu
Asian Flu
Hong Kong Flu
Bird Flu
Swine Flu
H3N2
H1N1
H2N2
H3N2
H5N1
H1N1
1889
1918
1957
1968
2004
2009
Hemagglutinin types = H1 –H17
Neuraminidase types = N1-N9
DNA Viruses
• Adenovirus – acute respiratory infections like
the common cold
• Poxvirus - cowpox, smallpox
• Herpesvirus – 100 herpesviruses are known!
Ex: HHV-1 and HHV-2 Simplexvirus – coldsores,
HHV-3 – chickenpox and HHV-4 – mono
• Papovavirus – warts. Some of these species are
capable of causing cancer.
Virus Replication
Viruses General Life Cycle:
Bacterial
Viruses
(phages)
1.Attachment
Animal
Viruses
2.Penetration/entry
Cell metabolism
SLOWS OR STOPS
Lysogenic
3.Biosynthesis
replication
Noninfectious
Lytic
4. Assembly/Maturation
Host Cell Dies
5.Release
Prophage – virus has
incorporated it’s DNA into
bacteria’s DNA
Multiplication of Animal Viruses
•
•
•
•
Attachment: Viruses attach to cell membrane
Penetration by endocytosis or fusion
Uncoating by viral or host enzymes
Biosynthesis: Production of nucleic acid and
proteins
• Maturation: Nucleic acid and capsid proteins
assemble
• Release by budding (enveloped viruses) or
rupture
Attachment, Penetration, Uncoating
• By pinocytosis
Figure 13.14a
Attachment, Penetration, Uncoating
• By fusion
Figure 13.14b
Multiplication of DNA Virus
Figure 13.15
RNA Viruses
Sense Strand (+ Strand) RNA Virus
Figure 13.17a
Antisense Strand (– Strand) RNA Virus
Figure 13.17b
Double-Stranded RNA Virus
Figure 13.17c
Multiplication of RNA-Containing Viruses
Figure 13.17
Multiplication of a Retrovirus
Figure 13.19
Viral escape – presence or absence of
envelope
• Two methods by which mature viruses escape
their host cell
1. Host cell lysis - releases naked or non-enveloped
viruses
2. Budding – virus passes through cell membrane –
takes part of host cell’s membrane – envelope is
formed around capsid
Budding of an Enveloped Virus
Figure 13.20
Budding of an Enveloped Virus
Figure 13.20
Growing Animal Viruses
• Animal viruses
may be grown
in living
animals or in
embryonated
eggs
Figure 13.7
Bacteriophages
Bacteriophages (Phages)
Figure 13.6 The complex shape of bacteriophage T4.
Head
Tail fibers
Tail
Base plate
A Viral One-Step Growth Curve
Figure 13.10
The Lytic Cycle
• Attachment: Phage attaches by tail fibers to
host cell
• Penetration: Phage lysozyme opens cell wall;
tail sheath contracts to force tail core and
DNA into cell
• Biosynthesis: Production of phage DNA and
proteins
• Maturation: Assembly of phage particles
• Release: Phage lysozyme breaks cell wall
Lytic Cycle of a T-Even Bacteriophage
1
2
3
Figure 13.11
The Lytic Cycle
• The lytic cycle is a phage reproductive cycle that
culminates in the death of the host cell
• The lytic cycle produces new phages and digests
the host’s cell wall, releasing the progeny viruses
• A phage that reproduces only by the lytic cycle is
called a virulent phage
• Bacteria have defenses against phages, including
restriction enzymes that recognize and cut up
certain phage DNA
Lytic Cycle of a T-Even Bacteriophage
4
Figure 13.11
Figure 13.8 The lytic replication cycle in bacteriophages.
The Lytic Cycle Progression
Figure 13.9 Pattern of virion abundance in lytic cycle.
Growing Lytic Viruses
• Viruses must be
grown in living
cells
– Bacteriophages
form plaques on
a lawn of bacteria
Figure 13.6
Results of Multiplication of
Bacteriophages
• Lytic cycle
– Phage causes lysis and death of host cell
– Can lead to Generalized transduction
• Lysogenic cycle
– Prophage DNA incorporated in host DNA
– Phage conversion
– Can lead to Specialized transduction
The Lysogenic Cycle
• The lysogenic cycle replicates the phage genome
without destroying the host
• The viral DNA molecule is incorporated into the
host cell’s chromosome
• This integrated viral DNA is known as a prophage
• Every time the host divides, it copies the phage
DNA and passes the copies to daughter cells
The Lysogenic Cycle
• An environmental signal can trigger the virus
genome to exit the bacterial chromosome and
switch to the lytic mode
• Phages that use both the lytic and lysogenic cycles
are called temperate phages
The Lysogenic Cycle
Figure 13.12
Generalized Transduction
2
3
4
5
6
Figure 8.28
Generalized Transduction
2
3
4
5
6
Figure 8.28
Specialized Transduction
Figure 13.13
Specialized Transduction
Figure 13.13
Viral Replication
Viruses General Life Cycle:
Bacterial
Viruses
(phages)
1.Attachment
2.Penetration/entry
Cell metabolism
SLOWS OR STOPS
Lysogenic
3.Biosynthesis
replication
Noninfectious
Lytic
4.Maturation
Host Cell Dies
5.Release
Prophage – virus has
incorporated it’s DNA into
bacteria’s DNA
Animal
Viruses
HIV
HUMAN IMMUNODEFICIENCY VIRUS
AIDS
• 1981: In United States, cluster of pneumonia
and Kaposi's sarcoma (cancer of skin & blood
vessels) discovered in young homosexual men
– The men showed loss of immune function
• 1983: Discovery of virus causing loss of immune
function – HIV
The Origin of AIDS
• Crossed the species barrier (from chimps &
monkeys) into humans in Africa in the 1930s
through animal butchering for food
• Patient who died in 1959 in Congo is the oldest
known case
• Spread in Africa as a result of urbanization
• Spread worldwide through modern
transportation and unsafe sexual practices
HIV Transmission
• HIV survives 6 hours outside a cell
• HIV survives less than 1.5 days inside a cell
• Infected body fluids transmit HIV via
– Sexual contact
– Breast milk
– Transplacental infection of fetus
– Blood-contaminated needles
– Organ transplants
– Artificial insemination
– Blood transfusion
Structure of HIV and Infection of CD4+ Cell
Figure 19.13
HIV Attachment
Figure 19.13
Fusion of the HIV w/Cell
HIV Entry
Figure 19.13
HIV Infection
http://www.johnkyrk.com/virus.html
Figure 13.19
Active HIV Infection in
+
CD4
T Cells
Latent virus
http://www.galaxygoo.org/biochem/hiv/h
ecycle.html
Figure 19.14b
Active HIV Infection in Macrophages
Figure 19.15b
Latent HIV Infection in Macrophages
Figure 19.15a
Vaccine Difficulties
Why?
Vaccine Difficulties
• Mutations – retroviruses mutate more often than
DNA viruses. Why?
– Hint: compare enzymes involved.
• Antibody-binding sites “hidden” when viruses
are latent
The Progression of HIV Infection
Figure 19.16
Worldwide Distribution of AIDS and HIV
14,000 new cases worldwide per day!
Figure 19.17
Chemotherapy
•
•
•
•
reverse transcriptase inhibitors
Protease inhibitors
Fusion inhibitors
HAART – highly active antiretroviral therapy
– Combination of drugs to counteract drug mutations
– Cannot eliminate latent viruses; goal is to reduce viral
load to level that immune system can handle
http://pharmaxchange.info/press/2011/01/hiv-life-cycle/
http://www.pbs.org/wgbh/evolution/library/10/4/l_104_06.html
http://www.pbs.org/wgbh/evolution/library/10/4/l_104_05.html
What antivirals did you find???
Other Ideas
• Lactobacillis in vaginal microbiota that can
produce bacteriocins that inhibit HIV
• Virus decoys – HIV binds decoy instead of CD4
• Boosting immunity – hormone to increase CD4
cells