Flashcards in Lecture #9: Viruses/The Archaea Deck (22):
A unique group of infectious agents whose distinctiveness resides in their simple acellular organization and pattern of multiplication.
Viruses are ubiquitous. Everywhere, in abundance. Target every type of living creature.
Move genes – between organisms, between groups, across generations. As much as 10% of the human genome is viral in origin.
Control population density. For single celled organisms, they are predators. Exert selective pressure.
Vectors. Deliver genes to target cells.
Biological Control Agents. Infect species likely to multiply quickly. Keep populations in check. Infect most effectively when hosts are at high density.
Why Are Viruses The Ultimate Dispersal Package?
Bare minimum. No fluid weight (no cytoplasm). Few, if any, enzymes (Teguments, Retroviruses = exceptions).
Commandeers host materials (ATP, nucleotides, amino acids) and host machinery (ribosomes, enzymes, possibly ER and Golgi).
Dispersed efficiently in air or by contact with living things or non-living things (fomites). A door handle that I touch while a virus is still infectious and then introduce into a mucous membrane is a fomite.
The simplest viruses are constructed of a nucleocapside. The nucleocapside is composed of nucleic acid, either DNA or RNA, held within a protein coat called the capsid.
The viral nucleic acid encodes viral proteins, some used to form the capsid. The capsid protects the viral genome and aids in its transfer between host cells. The proteins that form the capside are called protomers.
Virus Nucleic Acid
DNA – can be double-stranded or single-stranded.
RNA – can be double-stranded or single-stranded.
If RNA, can be a + or a – strand.
- If it is +, translated directly into viral proteins. Sense strand.
- If it is -, host cell must first create a complementary strand to use to make the proteins. In some, works through a DNA intermediate.
Many animal viruses and some plant viruses, and at least one bacterial virus are bounded by an outer membranous layer called the envelope. Animal virus envelopes usually arise from host cell plasma or nuclear membranes.
Shaped like hollow tubes with protein walls. The size of a helical capsid is influenced by both its protomers and the nucleic acid enclosed within the capsid. The diameter of the capsid is a function of the size, shape, and interactions of the protomers. The nucleic acid appears to determine its length because a helical capsid does not extend much beyond the end of the viral genome.
Most efficient way to enclose a space. A few genes, sometimes only one, can code for proteins that self assemble to form the capsid. In this way, a small number of genes can specify a large 3D structure.
Constructed from ring or knob shaped units called capsomers, each usually made of five or six protomers. Pentamers (pentons) have give protomers; hexamers (hexons) six. Pentamers are usually at the vertices of the icosahedron, whereas hexamers generally form its edges and triangular faces. In some RNA viruses, both the pentamers and hexamers of a capsid are constructed with only one type of subunit. In other viruses, pentamers are compsoed of different proteins than are the hexamers. Although many icosahedral capsides contain both pentamers and hexamers, some have only pentamers.
Mix of the two (Icosahedral and Helical), often with auxiliary parts.
Icosahedral head, helical collar, and tail proteins.
Tail injects the DNA (ds). Capsid remains outside, new DNA and capsids made by host, self-assembled in host and released.
Or bacteriophages, viruses that infect bacteria.
Because viruses need a host cell in which to multiply, 1st step is attachment (adsorption) to a host. Followed by entry of either the nucleocapside of the viral nucleic acid into the host.
Once inside the host cell, synthesis stage begins. During this stage, genes encoded by the viral genome are expressed. The viral genes are transcribed and translated. Allows virus to take control of host cell, forcing it to manufacture the viral genome and viral proteins.
Followed by assembly stage, during which new nucleocapsides are constructed by self-assembly of coat proteins with the nucleic acids.
Finally, during the release step, mature viruses escape the host.
Period where no intact infecting particle is present. Unique to viruses.
Eclipse Phase Can Be Diagnostic
- Lytic Viruses - Different periods of time from no detectable infectious particles to burst. Time when there are no intact virions.
- With Lysogenic Viruses (those with a dormant period, the lysogenic period), times between infection and burst vary. Months, years. May go into the active burst phase (lytic phase) due to a trigger—stress of some sort. Also Slow Release.
One that has only one option: to begin multiplaying immediately upon entering its bacterial host, followed by release from the host by lysis.
Has two options.
Upon entry into the host, the can multiply like the virulent phages and lyse the host cell.
Or they can remain within the host without destroying it. Many temperate phages accomplish this by integrating their genome into the host cell's chromosome. Bacteriophage lambda is an example of this type of phage.
The relationship between a temperate phage and its host cell.
The form of the virus that remains with its host is called a prophage, and the infected bacteria are called lysogens or lysogenic vacteria.
Lysogenic bacteria reproduce and in most other ways appear to be normal. However, they have two distinct characteristics. First is that they can't be reinfected by the same virus. The second is that they can switch from the lysogenic cycle to the lytic cycle. This results in host cell lysis and release of phage particles. This occurs when conditions within the cell cause the prophage to initiate synthesis of phage proteins and to assemble new virions, a process called induction.
Advantages of Lysogeny
First is that lysogeny allows a virus to remain viable within a dormant host. Bacteria often become dormant due to nutrient deprivation, and while in this state, they don't synthesize nucleic acids or proteins. In such situations, a prophage would survive but most virulent bacteriophages would not be replicated, as they require active cellular biosynthetic machinery.
The second advantage arises when there are many more phages in an environment than there are host cells, a situation virologists refer to as a high multiplicity of infection (MOI). In these conditions, lysogeny enables the survival of host cells so that the virus can continue to reproduce.
Infection of Eukaryotic Cells
Viruses can harm their eukaryotic host cells in many ways. An infection that results in cell death is a cytocidal infection. As with bacterial and archaeal viruses, this can occur by lysis of the host.
Viral growth doesn't always result in lysis. Some can establish persistent infections lasting many years. Eukaryotic viruses can cause microscopic or macroscopic degenerative changes or abnormalities in host cells and in tissues that are distinct from lysis. These are called cytopathic effects (CPEs).
Viruses use many methods to cause cytopathic and cytocidal effects.
The Archaea are Extremophiles
They live in habitats that are extremely hot (geothermal vents and pools), or extremely cold (in Arctic Ice, the hairs of polar bears), where the pH is extreme, where salt levels are high, or where there is extreme levels of radiation or intense sunlight.
As you might guess, they have specific adaptations for such extreme habitats.
Archaeal Plasma Membranes
Composed primarily of lipids that differ from bacterial and eukaryotic lipids in two ways. First, they contain hydrocarbons derived from isoprene units--five-carbon branched molecules. Second, they hydrocarbons are attached to glycerol by ether links rather than ester links. When two hydrocarbons are attached to glycerol, the lipids are called diether lipids. Usually the diether hydrocarbon chains are 20 carbons in length. Sometimes tetraether lipids are formed when two glycerol residues are linked by two long hydrocarbons that are 40 carbons in length. Cells can adjust the overall length of the tetraethers by cyclizing the chains to form pentacyclic rings. Phosphate-, sulfur-, and sugar-containing groups can be attached to the third carbons of the glycerol moieties in the diethers and tetraethers, making them polar lipids.
Despite these significant differences in membrane lipids, the basic design of archaeal membranes is similar to the other two--two hydrophilic surfaces and a hydrophobic core.
Archaeal Cell Walls
Before they were distinguished as a unique domain of life, the Archaea were characterized as being either gram+ or gram-. However, their staining reaction doesn't correlate reliably with a particular cell wall structure. Archaeal wall structure and chemistry differ from the bacteria. Archaeal cell walls lack paptidoglycan and exhibit considerable variety in terms of their chemical makeup.
The most common type of archaeal cell wall is an S-layer composed of either glycoprotein or protein. The layer may be as thick as 20-40 nm. Some methanogens, salt-loving archaea, and extreme thermophiles, have S-layer cell walls.
Other archaea have additional layers of material outside the S-layer. Some have a protein sheath external to it.
In some archaea, the S-layer is the outermost layer and is separated from the plasma membrane by an interesting molecule called pseudomurein.
Last type of archaeal cell wall doesn't have a S-layer. Instead these archaea have a wall with a single, thick homogenous layer resembling that in gram+ bacteria. These archaea often stain gram+.
Universal Start Sequence is AUG. In Eukarya and Archaeans, it specifies Methionine. In Bacteria, it specifies N-Formyl Methionine. (And organellar genes…)