Introduction to Virology Flashcards
The infectious unit of the virus is called the
Virus particle or virion
Virions contain a nucleic acid genome surrounded by a protective shell or coat of protein. The complex of protein and nucleic acid forms the
Nucleocaspid
Surrounded by an envelope, a lipid bilayer derived from host-cell membrane in which virus-encoded glycoproteins are inserted
Nucleocaspids
Enveloped viruses are distinguished by their sensitivity to
-Disrupts the lipid bilayer and destroys infectivity
Ether
Proteins of the nucleocapsid and envelope are
Structural proteins
Protects the genome and forms the delivery system: it binds a virion to its host cell and enables the genome to enter it
Nucelocapsid (and envelope if present)
Virion enzymes, unlike the abundant structural proteins, are present in only a few copies and are not essential to the structural integrity of the virion. They are referred to as
Non-structural proteins
Isolated virions are metabolically inert. They do not synthesize proteins or nucleic acids. If they contain enzymes, there are no substrates. Virions of many viruses can be
Crystallized
The type of viral genome dictates the replication cycle: the infecting genome must produce both
mRNA and new genomes
Viruses replicate only in living cells. Because of their limited genetic capacity, they are totally dependent on their host cells. This is called
Obligate intracellular parasitism
The intimate molecular interaction between virus and host means that a virus may be able to replicate only in cells of a particular species. This is referred to as
Species, tissue, or cell tropism
Cells in which a virus an replicate are said to be
Permissive
In non-permissive cells, infection does not result in production of new infectious virus particles; such infections are
Abortive
Replication of a virus requires its
Disassembly
Because of their small genomes, viruses must produce nucleocapsids from one or a few types of
Protein
There are only two solutions to the problem of enclosing a genome with only a single type of structural subunit. The subunits must be arranged in either a
Helix, or icosahedron
The protein subunits of nucleocapsids are held together by
Non-covalent bonds
Consist of a single protein subunit which assembles in a spiral or helix to form an open tube. Nucleic acid may be wrapped around the interior face of the tube, or enclosed within the wall
Helical Nucleocaspids
At some positions six adjacent subunits meet at a point, rather than five. The two types of cluster are called
Pentons and Hexons
In some viruses subunits are sufficiently flexible to be used in both places. This is called
Quasi-equivalent pairing
A few of the largest viruses have nucleocapsids which, although geometrically regular, have no obvious symmetry. These are called
Complex nucleocaspids
Viruses are visualized in the EM by
Negative staining
After negative staining, virus coats often show regular arrays of
Protrusions (capsomeres)
Have single-stranded RNA genomes of negative polarity
Mono-negavirales
Intact skin is impermeable to
Viruses
Many viruses are transmitted via the
Respiratory route
The coat of a virus contains proteins which specifically bind to cell surface
Receptors
These receptors are not present to facilitate viral infection, but to carry out specific
Physiologic functions
Binds to CD21, a C3b receptor on B cells
Epstein-Barr virus
Binds to CD4 of helper T cells. Distribution of CD4 determines which cells it can infect
HIV
Enter cells by one of two routes: (1) direct fusion of the viral envelope with the plasma membrane, or (2) receptor-mediated endocytosis
Nucleocaspids
This process may be catalyzed by one or more
Fusion proteins
In viruses which use the second route, acidification of the endosome may be required to cause a conformational change, required for fusion, in the
Fusion protein
Exposure of the genome in a form competent for transcription/replication is called
Uncoating
For nuclear replication, the virus core or nucleocapsid must be transported into the
Nucleus
Transcription of viral genes, synthesis of viral proteins, and assembly of new virions occurs in which two phases?
- ) Early phase
2. ) Late phase
Where viral proteins are made which replicate the viral genome
-Some viruses also produce proteins which block synthesis of host-cell nucleic acids and/or proteins
Early phase
Where new structural proteins are made and new virions assembled
Late phase
Have regulatory mechanisms which cause a switch from production of early to late proteins after genome replication has begun
Some viruses
During the interval between disassembly of the infecting virion and assembly of the first progeny virions, an infected cell contains no
Infectious virions (called the eclipse period)
Some virion genomes may contain suffered deletion/mutation of their genetic material, so that after infection no infectious progeny are produced. Such virions are
Defective
Progeny virions of enveloped viruses assemble at, and are extruded from, cellular membranes. This is termed virus
Budding
The replication cycle of Polio virus takes
6-8 hours
Assembled and released by budding, at the plasma membrane or internal membranes
Enveloped Viruses
Enveloped viruses are not infectious until they have acquired their
Envelope
Virus infection may itself kill cells: new virions of some viruses can exit the host cell only by its
Lysis
The immune response, both innate and acquired, may kill
Infected cells
Cell death and the immune response produces inflammation, and this in itself may
Damage tissue
Crucial to the early limitation of viral multiplication
Interferon system
Interferons are cytokine made by cells in response to
Viral infection
An important stimulus for interferon production is
Double-stranded RNA
Binds to its receptors to kill infected cells before virus release, and to stimulate uninfected cells to produce antiviral defenses
Interferon
Another defense against viruses is the apototic response of infected cells. Many viruses combat this by producing proteins which block
Apoptosis
In order to clear the initial viral infection, we usually require production of
CTL
Many viruses inhibit synthesis of MHC proteins or their export to the plasma membrane. These viruses are combated by
NK cells
Other viruses establish infections, in which viral genomes persist in infected cells but few or no virus proteins are produced. These are called
Latent infections
These >common cold= viruses are transmitted by the respiratory route and multiply in the epithelium of the nasal mucosa
Rhinovirus
After rhinovirus infection, the asymptomatic incubation period lasts
2-4 days
During the early symptomatic period large numbers of rhinovirus particles are present in
Nasal secretions
Appears in serum and nasal secretions 7-21 days after rhinovirus infection, after virus numbers have already begun to fall
Neutralizing antibody
The rhinovirus is classified as a
Local infection
The varicella virus is classified as a
Disseminated infection
Initial infection is by the respiratory route
Varicella Virus
During the incubation period varicella virus multiplies in the respiratory epithelium and infects cells of regional
Lymph nodes
Released virus is transported via the bloodstream (primary viremia) to cells of the
Reticuloendothelial system
The end of the incubation period and the beginning of symptoms (10-21 days after inital infection) is marked by a
Secondary virema
When the virus is transported back to the respiratory epithelium [patients are infectious during this stage], to skin, where it infects epithelial cells to produce the characteristic rash, and to dorsal root ganglia, where it becomes latent in sensory neurons
Secondary viremia
Neutralizing antibody in plasma and secretions appears at about the same time as the
Rash
Clearance of the infection depends critically on generation of
CTL
The more rapid the CTL response the milder and less extensive is the
Rash
Infectious virions can be detected by exposing a monolayer of susceptible cells to a sample of virus diluted until only a small number of virions are
Present
When mammalian cells are used, the monolayer is overlaid with soft agar so that when infected cells release virions, they spread only
Locally
The small number of initially-infected cells release new virus that infects and kills neighboring cells. After a few days, each focus of infection creates an area of cell death called a
Plaque
Each plaque stems from a single
Virion
Standard cell cultures are in small flat-sided bottles or petri dishes, or as monolayers on coverslips in small
Shell vials
What are the two types of cells used for isolation of viruses?
Primary cultures and Cell lines
Derived directly from samples of human tissue
Primary cultures
Cells in primary culture are normal in nearly all respects but will not proliferate
Indefinitely
They require stimulation by growth factors in serum and contact with extracellular matrix and are inhibited by contact with their neighbors
Primary cultures
Have been adapted to long-term or continuous culture but may not be normal in all respects
Cell lines
Infection may lead to cell death or characteristic changes in
Cell shape
Contain proteins which allow viral envelopes to fuse with cellular plasma membranes
Viral envelopes
When these proteins appear on the plasma membranes of infected cells, they can cause infected cells to fuse with neighboring uninfected cells, creating
Giant cells or syncytia
Aggregates of virus particles or components visible under the light microscope after staining
Inclusion bodies
Multiplies in the cytoplasm and its inclusion bodies (Negri bodies) are cytoplasmic
Rabies Virus
Herpes viruses multiply in the nucleus and their inclusions are
Intra-nuclear
Viral nucleic acid can be detected by
PCR or hybridization
Results in production of virus-specific humoral and cell-mediated immune responses
Viral infection
Methods include complement fixation, neutralization, ELISA, and hemagglutination inhibition (HI)
Viral serology
Complement-fixing antibodies are often made to antigens common to a group of
Viruses
Often highly specific to an individual virus
Neutralizing antibodies
May rise and fall at different times after infection. This may be useful in establishing how long an infection has been going on
Antibody titer
Because of immunological memory, use of virus-specific IgG to diagnose current infection requires comparison of titer between two samples, taken
10-14 days apart
Because the first sample is often taken while the patient is acutely ill and the second while the patient has begun to recover, the samples are often referred to as
Acute and convalescent sera