Human Microbiology (ii)
First post in the series here. You can buy it here. I put it away temporarily a while ago, but this week I tried having another go at it. I’ve now read something like 2/3rds of the book, and I’ve taken a look at almost all chapters – which also means that I’ve skipped some stuff here and there. It’s a good book, and it’s actually reasonably accessible, though it’s not easy. Most of the stuff in the first post was about bacteria, but of course the book also has some stuff about viruses and fungi. Some more material below, I’ve decided to limit myself to dealing with stuff related to viruses in this post. They are actually quite interesting (things? …buggers?):
i. “Viruses are succesful parasites; they infect all the main types of living organisms from animals, plants and insects to fungi and bacteria. Viruses that infect bacteria are called bacteriophages.
Viruses are obligate intracellular parasites. They have an absolute requirement on the host cell for manufacture of new virus components. Viruses do not multiply by binary fission but instead are assembled from component parts (nucleic acid and protein). This can only occur inside the host cell. Hence, viruses are inert outside of their hosts. With no need for a basal metabolic activity to retain viability, viruses have no need to carry ribosomes or other organelles or metabolic pathways. They simply are particles that can be copied and built by the cells that they infect. […]
In the process of becoming entirely parasitic, certain viruses have lost the minimum amount of genetic information such that they are unable to replicate outside the host cell unless aided by another virus. Such viruses are called defective viruses. […] Certain viruses have lost so much nucleic acid that they are simply infectious strands of RNA. Called viroids, these agents lack even a protective protein coat surrounding the RNA strand yet are able to infect plants, transmitted following mechanical abrasion of the plant surface. […]
Viruses resemble living organisms in that they have a genome and are able to replicate and evolve. Indeed, they have biological properties such as particular host ranges, routes of transmission and tissue tropism. Viruses, however, do not create or store free energy in compounds such as ATP and have no intrinsic metabolic activity outside their host cells (unlike spores or seeds) and are therefore not alive, at least for part of their existence. These comparisons place viruses in between chemicals and true living organisms. Attempting to include the important features, a definition of a virus is thus:
A microscopic organism that invades and only reproduces inside living cells. Viruses possess one type of nucleic acid, are unable to replicate by binary fission but are assembled and do not undertake independent energetic metabolism.” […]
“One of the most unusual features of viruses is the presence of only one type of nucleic acid. Whereas other organisms possess both DNA and RNA, viruses have only one nucleic acid, DNA or RNA, never both.”
ii. “The virus-infected cell should be seen as a controlled hijacking of the normal cell by an intruder. The replication strategy will depend on the type of genome, and the release of the virus will determine the pattern of infection within the host.
A number of differences are apparent when comparing viral replication with bacterial replication (Figure 3.8) [a good figure, not going to draw it]. A virus replicates itself from scratch, starting from the transcription of its nucleic acid, whereas a new bacterial cell is derived from a pre-existing bacterial cell as it doubles its cellular components and divides, a process not driven from nucleic acid transcription. This is partly reflected in the time taken to form new viruses and bacteria. A bacterium dividing in culture can be a relatively short event (20 minutes for Esch. coli), whereas the replication of a virus takes roughly 8 hours to complete. Whilst the bacterial cell doublings can be estimated during exponential bacterial growth, numbers of viruses produced from a single virus within one host cell cannot be predicted. The integration of the host cell machinery with that of the virus makes the targets for antiviral compounds all the more difficult.” […]
The replication of the virus can be divided into five stages, reflecting the general sequence of events:
*transcription of the genome,
*virus release. [the book spends 8 pages on these five concepts, so I’m not going into details about this part here.
iii. “If a virus grows intracellularly and does not kill the cell one might expect that infected cells remain indistinguishable from uninfected cells. Fortunately, certain viruses betray their presence by causing such disruption to the cells that they cause visible cytopathic effect (CPE). This is a general term for any alteration in the morphology of the cells caused by the virus. Not all viruses induce cytopathic effects. […] Examples of various cytopathic effects are shown in Figure 3.14, and discussed below.
*Formation of inclusion bodies. Unusual organelles may appear within virus-infected cells and are described as ‘inclusion bodies‘. […]
*Changes in the shape of the infected cells. […]
*Cell lysis. The lysis of cells by a virus is a feature of several viruses when grown in cell lines. The pattern of the gaps left by the detached dead cells from the cell monolayer is called a ‘plaque’. […] Lytic viruses cause the cell to disrupt, typically when non-enveloped virus particles are released. Clearly this is fatal to the cell in question.
*Cell fusion. Infected cells may fuse and form multinucleate cells called syncytia when infected with certain viruses. […]
iv. “At a conservative estimate, there are at least thirty different viruses from fifteen taxonomic families that are common causes of human illness. This number does not take into consideration the serological types that exist in many of these viruses. So the common cold we are taking as one virus, whereas there are over eighty serological types of rhinovirus. As every human will be infected by viruses in their lifetime, we must concede that viruses are efficient parasites of humans.” […]
“Because it is only those people with symptoms who come to our attention, it is easy to overlook the fact that most viral infections are asymptomatic. […] The proportion of susceptible people who develop illness from those who are infected is called the attack rate”
The book makes it clear in a table and a figure neither of which I can easily reproduce that there are basically four types of viral infections, when using duration as the decision parameter: Acute, persistent, latent and slow. Examples given of the four types are: Rhinovirus (common cold), chronic hepatitis B, Herpes simplx and BSE (mad cow disease). Their strategies differ somewhat:
“The acute infections rely on rapid multiplication of virus in order to manufacture and shed (transmit) new virus before the host has had time to mount a neutralising immunity. […] Persistent infections in the host (not the environment) are those in which the virus is not eliminated but, having established itself, will persist for the lifetime of the host. The virus is either replicating at a very low level continually, such as chronic hapatitis virus infections, or is latent for most of the time but periodically undergoes a short burst of full replication in which infectious virus is manufactured and released, e.g. Herpes simplex in cold sores. Many persistent virus infections are acquired as children with little or no pathology and then persist for life.” […]
“Viruses have adopted various strategies to out-manoeuvre the host, in particular to evade or suppress the immune response that attempts to develop antiviral products. It is useful to consider the broader strategies before looking at cellular mechanisms.
*Evasion of immune response. Viruses can replicate in tissues that are relatively protected from surveillance by immune cells (e.g. brain, dermis). Alternatively, they can avoid extracellular states in the course of infection. […]
*Suppression of immune response. Some virus infections infect the immune cells that mount the immune response in order to suppress them. […]
The following list illustrates how viruses have attempted to modulate various points of the immune response.
*Minimise recognition by the host. For viruses that cause systemic infections, the first entry of virus into the bloodstream during a viraemic phase will attract the attention of Complement components. Certain viruses produce molecular mimics (homologues) of Complement components which will block the Complement cascade attacking the free virion. These homologues are termed viroceptors. Mimicry is also used by enveloped viruses which include host proteins in the viral envelope to mask their recognition as ‘foreign’. […]
*Inhibit production of interferon. Interferon production is an important early step in the defence against viral infections. Viruses need to interfere with the action of interferon to establish an infection. One way to counter the action of interferon, is for viruses to secrete molecular mimics of IFN receptors. In this way IFN binds to the competing mimic receptor, rather than real receptor on the virus-infected cell. […]
*Modulation of cytokine action. […]
*Prevent apoptosis. Apoptosis, programmed cell suicide, occurs only if a cell receives a signal to proceed. That signal may be triggered by the presence of a virus. In general, viruses try to prevent the cell from carrying out this self-destruction and numerous examples exist of viruses producing proteins that inhibit apoptosis.”
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