5. Lecture Flashcards
describe the multiplication cycle of viruses
- adsorption (attachment to the host cell)
- penetration (entry into the host cell)
- decapsidation (nucleic acid release)
- eclipse (expression of the genetic information)
- transcription, translation and nucleic acid replication
- maturation (assembly of progeny virions)
- release (evacuation from the host cell)
how many virions/cell can be produced
102 – 106 virion/cell
- > new cells, new cycles
- > log phase
cell surface receptor
10⁴⁻⁵ /cell (stable)
genetically coded (ie. H19 chromosome poliovirus
H3 chromosome HSV)
•usually already expressed in the embryo, some after birth
•necessary for cellular functions
(ie. CD4 – HIV, acetylcholine receptor – rabies virus)
virus surface antireceptor
more variable than the cell surface receptor as they adapt them during their evolution
related viruses usually target the same cell surface receptor
sometimes non-related viruses have the same receptor
how is the connection btw. receptor and antireceptor made
both negatively charged -> repulsion, collision by chance
reversible connection -> cations neutralize the electrostatic power -> irreversible connection -> chemical bonds between theproteins
penetration: energy use
energy-dependent: 4 × activation energy than adsorption
only possible in living cells
only possible over +4°C
types of penetration
translocation
endocytosis
membrane fusion
translocation
„trapdoor” mechanism, amorphous RNA-protein complex
endocytosis
(most non-enveloped viruses + herpes, pox)
cell nutrition endosome -> phagolysosome -> decapsidation
membrane fusion
(only enveloped viruses)
• virual fusion (F) protein induced
• the viral envelope merges into the cytoplasmic membrane of
the host cell; only the nucleocapsid gets into the cytosol
alternative forms of penetration
- injection
- sexfimbria
- passive penetration
injections
(tailed bacteriophages):
• lysozyme enzyme + contractile proteins
sexfimbria
(ribophages):
•lack of cellular wall „bacterial sexual disease”
passive penetration
(plant viruses):
•cellular wall injuries, arthropod bites
decapsidation
uncoating:
• Release of the nucleic acid from the capsid
• Dangerous for the virus, but necessary for the transcription (capsid = protection) so NA is reachable
strategies of decapsidisation
•Use of cellular proteases (in lysosomes)
->Viral uncoating proteins (ie. poxviruses)
•Partial decapsidation
->hiding the nucleic acid until the early virus protein production (two capsid layer – only outer is decomposed, inner, holes are made to reach double stranded RNA )
(ie. DNA viruses in the nucleus, reo, orthomyxo,
paramyxoviruses)
•Sometimes simultaneous penetration and decapsidation (ie. by translocation, injection)
eclipse
The expression and copy of the viral genetic information
•transcription, translation, nucleic acid replication of NA
•different strategies according to the type of the nucleic acid
– the Baltimore-system
the baltimore system
virus classification system that groups viruses into families, depending on their type of genome (DNA, RNA, single-stranded (ss), double-stranded (ds), etc..) and their method of replication.
maturation
Polypeptide → protein
• Glycosylation, dimer formation, antigen development
• at the ER surface or Golgi
Virus assembly
• Usually at the site of replication for protection
– RNA viruses + Pox, Asfarviridae in cytoplasm
– other DNA viruses in nucleus
• protein transport – may evolve inclusion bodies for tp.
• nucleic acid signal connects to the capsomers
envelope and matrix proteins are acquired from cellular membranes
mistake frequency in virus assembly
frequent
→the production of incomplete virions usually about 70%
methods of virus assembly
The nucleic acid enters into the capsid: icosahedral
The capsomers surround the nucleic acid: helical
regulation of virus assembly
scaffolding proteins regulate the assembly
virus release of non-enveloped viruses
cytolysis
rapid (Picornav.) / slow (Parvov.) / apoptosis (Adenoviridae)
