Biological Sciences
Latent Viruses
Latent viruses are those that remain dormant within a host cell without causing any symptoms of infection. These viruses can reactivate and start replicating, leading to the onset of disease. Latent viruses are capable of persisting in the host for extended periods, and their reactivation can be triggered by various factors such as stress, immunosuppression, or hormonal changes.
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10 Key excerpts on "Latent Viruses"
eBook - PDF- Nigel J. Dimmock, Andrew J. Easton, Keith N. Leppard(Authors)
- 2015(Publication Date)
- Wiley-Blackwell(Publisher)
Academic Press, London. Ondondo, B. O. 2014. Fallen angels or risen apes? A tale of the intricate complexities of imbalanced immune responses in the pathogenesis and progression of immune-mediated and viral cancers. Frontiers in Immunology 5, 90. Roizman, B., Whitley, R. J. 2013. An inquiry into the molecular basis of HSV latency and reactivation. Annual Reviews of Microbiology 67, 355–374. Chapter 17 Mechanisms in virus latency Latent infections are an important facet of the interaction of certain viruses with their hosts. The ability to establish a latent infection means that the virus can maintain its genome in the host for the entire life of the host, being reactivated periodically to produce new viruses which can infect new hosts. This can be seen as a highly evolved virus–host interaction. As James Lovelock, originator of the Gaia hypothesis, put it: “An inefficient virus kills its host. A clever virus stays with it.” Chapter 17 Outline 17.1. The latent interaction of virus and host 17.2. Gene expression and the lytic and lysogenic life of bacteriophage λ 17.3. Herpes simplex virus latency 17.4. Epstein-Barr virus latency 17.5. Latency in other herpesviruses 17.6. HIV-1 latency of their associated diseases and potential therapies. It also has relevance to the potential use of animal viruses, such as the defective parvovirus adeno-associated virus, as vectors for gene therapy. The establishment of latency represents the ultimate parasitic interaction in virology, with the virus able to co-exist with a host which, in most cases, gains no obvious advantage. A common perception of virus infection is that the only possible outcome is an immediate and rapid production of progeny virus particles. While this is the most common result of infection it is not the only one, as described in Chapter 16.
eBook - PDF- N A Khan(Author)
- 2008(Publication Date)
- CRC Press(Publisher)
93 5.3 Persistent Infections In these infections, the virus is not cleared from the human body and is maintained in the host cells for longer periods of time. These are several types of persistent infections that differ in their mechanisms and are described below. 5.3 .1 Chronic Infection In these infections, the virus targets their host cells and replicates inducing a low level of symptoms. However, new virions are controlled by innate and acquire host immune system (in particular, antibodies and T-cells). In chronic infections, there is a continued presence of infectious virions. This is associated with long incubation periods followed by progressive disease with the clear onset of clinical symptoms, e.g., Hepatitis B virus. 5.3.2 Latent Infections In latent infections, the virus produces an acute infection and becomes latent with limited replication. The virus is maintained in non-dividing or rarely dividing cells, e.g., Herpes simplex virus. Viruses are usually not detectable during the latent period, however, they are able to reactivate themselves in response to diverse signals (e.g., heat, ultraviolet irradiation, immune suppression, chemotherapy, etc.). 5.3.3 Tumourigenic Infections In these infections, viruses may or may not be released from the host cells. Viral proteins inactivate host cell tumour suppresser proteins (e.g., Eb, p53) resulting in impaired cell cycle. Examples include T antigens of papova viruses, E6, E7 of papilloma viruses, and Epstein-Barr virus. This results in the transformation of the cell to become immortalized. These, transformed cells, have reduced requirement for growth factors and become cancerous, i.e., grow forever. 5.3.4 Progressive Infections These infections take years to show any clinical symptoms. They normally begin with influenza-like symptoms and become latent. During the latent period, they propagate infectious particles. Once reactivated, they overwhelm the immune system, e.g., HIV.
eBook - PDF- Edward K. Wagner, Martinez J. Hewlett, David C. Bloom, David Camerini(Authors)
- 2009(Publication Date)
- Wiley-Blackwell(Publisher)
In such infec- tions, virus replication closely correlates with the cell’s differentiation state, and the virus can express genes that delay the normal programmed death (apoptosis) of such cells in order to lengthen the time available for replication. The distantly related polyoma viruses, BK virus and JC, induce chronic infections of kidney tissue. Such infections are usually asymptomatic and are only characterized by virus shedding in the urine; however, in immunosuppressed individuals infections of the brain and other organs can be seen. Thus, these persistent viruses have a role in the morbidity of late stage AIDS and in persons undergoing immunosuppression for organ transplants. Herpesvirus infections and latency As detailed in Chapter 17, Part IV, hallmarks of herpesvirus infections are an initial acute infection followed by apparent recovery where viral genomes are maintained in the absence of infectious virus production in specific tissue. Latency is characterized by episodic reactivation (recrudescence) with ensuing (usually) milder symptoms of the original acute infection. Example viruses include HSV, EBV, and VZV. In a latent infection, the viral genome is maintained in a specific cell type and does not actively replicate. HSV maintains latent infections in sensory neurons, whereas EBV main- tains itself in B lymphocytes. Latent infections often require the expression of specific virus genes that function to ensure the survival of the viral genome or to mediate the reactivation process. Reactivation requires active participation of the host. Immunity, which normally shields the body against reinfection, must temporarily decline. Such a decline can be triggered by the host’s reaction to physical or psychological stress. HSV reactivation often correlates with a host stressed by fatigue or anxiety. VZV reactivation leads to shingles, a very painful recrudescence throughout the sensory nerve net serving the site of the latent virus.
eBook - ePub- Nigel J. Dimmock, Andrew J. Easton, Keith N. Leppard(Authors)
- 2015(Publication Date)
- Wiley-Blackwell(Publisher)
+ T lymphocytes per person may be infected in this way. The latent virus can reactivate at any time though the stimuli for this are not well understood. This is important as most active virus multiplication, but not the latent virus infection, can be eliminated by chemotherapy (see Section 21.6). Thus, the latent infection acts as a reservoir from which virus can reappear if antiretroviral therapy is stopped. When this occurs, the levels of infectious virus in the body often exceed those prior to the treatment and there is a greatly enhanced likelihood of drug-resistant viruses appearing due to selection pressures. This means that the current therapy regime has to be maintained for life, with the attendant difficulties of expense, toxicity, non-compliance, or the eventual breakthrough of resistant mutants.Key Points
- Latency is an outcome of infection for certain viruses and is a state defined by the presence of viral genome without the production of infectious virus, but in which it is possible to reactivate a lytic infection.
- Among animal viruses, all herpesviruses have the ability to establish latent infections.
- The pattern of gene expression during latency is different to that seen during an acute infection: fewer virus genes, and sometimes no genes, are expressed during latency.
- In phage λ the establishment of latency is determined by a balance between the action of gene activators and gene repressors.
- In HSV-1 only RNA from the LATs and micro RNAs are seen during latency. In the other herpesviruses, several virus proteins may be produced during latency.
- Latency requires suppression of the early steps in the cascade of lytic gene expression.
- Following reactivation, infectious virus is produced from latently infected cells.
- In animals, the immune system is key in dealing with reactivation of infection.
Questions
- Consider the control of lysogeny in bacteriophage lambda and compare this with the gene expression of herpesviruses during the establishment and maintenance of latency.
- Discuss the potential outcomes of infection of humans with herpesviruses and describe the processes which control and determine the various stages of the infection.
Further Reading
- Johnson, A. D., Poteete, A. R., Lauer, G., Sauer, R. T., Ackers, G. K., Ptashne, M. 1981. λ repressor and cro-components of an efficient molecular switch. Nature (London)
eBook - ePub- Martinez J. Hewlett, David Camerini, David C. Bloom(Authors)
- 2021(Publication Date)
- Wiley-Blackwell(Publisher)
acute infections result in clearance of virus, this does not invariably happen. While infections with influenza virus, cold viruses, polioviruses, and poxviruses resolve with virus clearance, herpesvirus infections result in a lifelong latent infection. During the latent period, no infectious virus is present, but viral genomes are maintained in certain protected cells. Periodically, a (usually) milder recurrence of the disease (reactivation or recrudescence) takes place upon suitable stimulation.In distinct contrast, measles infection resolves with loss of infectious virus, but a portion of the viral genome can be maintained in neural tissue. This is not a latent infection because the harboring cells can express viral antigens, which lead to lifelong immunity, but infectious virus can never be recovered.Other lasting types of virus‐induced damage can be much more difficult to establish without extensive epidemiological records. Chronic liver damage due to hepatitis B virus infection is a major factor in hepatic carcinoma. Persistent virus infections can lead to immune dysfunction. Virus infections may also result in the appearance of a disease or syndrome (a set of diagnostic signs and symptoms displayed by an affected individual) years later that has no obvious relation to the initial infection. It has been suggested that diseases such as diabetes mellitus, multiple sclerosis, and rheumatoid arthritis have viral etiologies (ultimate causative factors). Virus factors have also been implicated in instances of other diseases such as cancer and schizophrenia.QUESTIONS FOR CHAPTER 2
- A good general rule concerning the replication of RNA viruses is that they require what kind of molecular process?
- What is the role of a vector in the transmission of a viral infection?
- It is said that viruses appear to “violate the cell theory” (“cells only arise from preexisting cells”). To which phase of a virus life cycle (growth curve) does this refer? What is the explanation for this phase of the growth curve?
eBook - PDF- Nina Parker, Mark Schneegurt, Anh-Hue Thi Tu, Brian M. Forster, Philip Lister(Authors)
- 2016(Publication Date)
- Openstax(Publisher)
(credit: modification of work by NIAID, NIH) Chapter 6 | Acellular Pathogens 257 • Is RNA-dependent RNA polymerase made from a viral gene or a host gene? Persistent Infections Persistent infection occurs when a virus is not completely cleared from the system of the host but stays in certain tissues or organs of the infected person. The virus may remain silent or undergo productive infection without seriously harming or killing the host. Mechanisms of persistent infection may involve the regulation of the viral or host gene expressions or the alteration of the host immune response. The two primary categories of persistent infections are latent infection and chronic infection. Examples of viruses that cause latent infections include herpes simplex virus (oral and genital herpes), varicella-zoster virus (chickenpox and shingles), and Epstein-Barr virus (mononucleosis). Hepatitis C virus and HIV are two examples of viruses that cause long-term chronic infections. Latent Infection Not all animal viruses undergo replication by the lytic cycle. There are viruses that are capable of remaining hidden or dormant inside the cell in a process called latency. These types of viruses are known as Latent Viruses and may cause latent infections. Viruses capable of latency may initially cause an acute infection before becoming dormant. For example, the varicella-zoster virus infects many cells throughout the body and causes chickenpox, characterized by a rash of blisters covering the skin. About 10 to 12 days postinfection, the disease resolves and the virus goes dormant, living within nerve-cell ganglia for years. During this time, the virus does not kill the nerve cells or continue replicating. It is not clear why the virus stops replicating within the nerve cells and expresses few viral proteins but, in some cases, typically after many years of dormancy, the virus is reactivated and causes a new disease called shingles (Figure 6.13).
eBook - ePub- David P. Clark(Author)
- 2009(Publication Date)
- Academic Cell(Publisher)
When instead, the virus divides in step with the host chromosome, this is known as lysogeny and a cell containing such a virus is a lysogen. The term latency means the same as lysogeny but is usually used when referring to animal cells. In Chapter 16 we discussed the close relationships between plasmids and viruses. Some gene creatures can choose to live either as a plasmid or as a virus. Some plasmids are probably derived from viruses that have lost the ability to grow lytically. Conversely, some viruses may have evolved from plasmids that obtained the genes for lytic growth, either from another virus or, over a longer period, from the host cell. Viruses may replicate aggressively, killing the host cell. Alternatively, they may limit themselves to duplicating their genome in step with cell division. Lysogeny or latency means that the virus has decided to divide in step with the host cell instead of killing it. It does not necessarily mean the virus has decided to live as a plasmid. Many cases of lysogeny or latency are caused by integration of the virus DNA into a host cell chromosome. Such an integrated virus is known as a provirus (or prophage in the case of bacterial viruses). The virus DNA becomes a physical part of the chromosome and is replicated when the chromosome divides. The bacterial virus lambda (λ), which infects the bacterium E. coli, recognizes and integrates into a special sequence of DNA on the chromosome of its host cell, known as attλ (λ attachment site). Integration occurs by site-specific recombination as described in Ch. 14. This allows lambda to occasionally pick up and carry bacterial genes as described in the chapter on bacterial genetics (Ch. 18). Some animal viruses, such as the herpes viruses, also insert themselves into the chromosomes of their host cells. Some have special recognition sites, while others insert at random
eBook - PDF- Julianne Zedalis, John Eggebrecht(Authors)
- 2018(Publication Date)
- Openstax(Publisher)
Animal viruses cause a variety of infections, with some causing chronic symptoms (hepatitis C), some intermittent symptoms (Latent Viruses such a herpes simplex virus 1), and others that cause very few symptoms, if any (human herpesviruses 6 and 7). Oncogenic viruses in animals have the ability to cause cancer by interfering with the regulation of the host cell cycle. Viruses of plants are responsible for significant economic damage in both agriculture and plants used for ornamentation. 21.3 Prevention and Treatment of Viral Infections Viruses cause a variety of diseases in humans. Many of these diseases can be prevented by the use of viral vaccines, which stimulate protective immunity against the virus without causing major disease. Viral vaccines may also be used in active viral infections, boosting the ability of the immune system to control or destroy the virus. A series of antiviral drugs that target enzymes and other protein products of viral genes have been developed and used with mixed success. Combinations of anti-HIV drugs have been used to effectively control the virus, extending the lifespans of infected individuals. Viruses have many uses in medicines, such as in the treatment of genetic disorders, cancer, and bacterial infections. 21.4 Other Acellular Entities: Prions and Viroids Prions are infectious agents that consist of protein, but no DNA or RNA, and seem to produce their deadly effects by duplicating their shapes and accumulating in tissues. They are thought to contribute to several progressive brain disorders, including mad cow disease and Creutzfeldt-Jakob disease. Viroids are single-stranded RNA pathogens that infect plants. Their presence can have a severe impact on the agriculture industry. REVIEW QUESTIONS 1. Viruses were first discovered after the development of the porcelain filter, called the Chamberland-Pasteur filter. How did the porcelain filter enable scientists to discover viruses? a.
- Lois N. Magner(Author)
- 2009(Publication Date)
- Praeger(Publisher)
Viruses differ considerably in the size of their genome and the time it takes to undergo replication. For example, some bacteriophages produce new viral particles in less than an hour, whereas some animal viruses take several days to complete the process. The origin of viruses is obscure, but they may have evolved from microorganisms that lost many of their cellular components or from genes that escaped from an ancestral cell and gained the ability to infect other cells. The behavior of viruses, even those that only attacked bacteria, proved to be more complicated than originally anticipated. During the 1940s, scientists were able to demonstrate the existence of two quite different groups of bacteriophages: lytic phages and lysogenic phages. Lytic phages take over a bacterial cell, replicate, and lyse the host cell to release a burst of new phages. Instead of immediately replicating and killing their target cells, lysogenic phages can either replicate in their target cell or integrate their DNA into the host’s DNA. In this case, the phage remains hidden in the genome of the host and its daughter cells until some stimulus triggers its reactivation. The existence of lysogenic phages was unknown to early phage workers, who assumed that all phages simply attacked and killed their bacterial targets. Eventually, researchers discovered that some of the viruses that cause disease in humans, such as the herpes virus, are also capable of establishing latent infections in human cells. After remaining dormant for long periods, a latent virus may become active and begin to replicate, producing new viruses that attack other cells. The French microbiologist Andr´ e Lwoff, who won the 1965 Nobel Prize for his work on lysogeny, was primarily interested in the physiology, biochemistry, and life cycle of microorganisms. Ultimately, Lwoff’s interest in lysogeny as the prototype for persistent, but hidden infections led to work on oncogenes, cancer-causing genes that
eBook - PDFMicrobiology
Principles and Explorations
- Jacquelyn G. Black, Laura J. Black(Authors)
- 2018(Publication Date)
- Wiley(Publisher)
And the polioviruses destroy nerve cells during the re- lease process. Latent Viral Infections Many individuals experience the recurrence of skin eruptions commonly called cold sores or fever blisters. These are caused by the herpes simplex virus, a mem- ber of the herpesviruses. As we saw earlier, these are dsDNA viruses that can exhibit a lytic cycle. They can also remain latent within the cells of the host organism throughout the individual’s life—not in the skin cells we associate them with, but in the nerve cells. When acti- vated, whether by a cold or fever or by stress or immu- nosuppression, they once again replicate resulting in cell lysis. The ability to become latent is held by all of the her- pesviruses. Another herpesvirus, the one that’s respon- sible for chickenpox, can also remain dormant within the central nervous system. When it becomes activated, usu- ally due to changes in cell-mediated immunity, the virus causes a rash to form along the nerve where it lay latent. This reactivation is known as shingles. Many individuals carry these viruses throughout their lives, never exhibit- ing any symptoms. CULTURING OF ANIMAL VIRUSES Development of Culturing Methods Initially, if a virologist wanted to study viruses, the viruses had to be grown in whole animals. This made it difficult to observe specific effects of the viruses at the cellular level. In the 1930s, virologists discovered that embryonated (intact, fertilized) chicken eggs could be used to grow herpesviruses, poxviruses, and influenza viruses. Although the chick em- bryo is simpler in organization than a whole mouse or rab- bit, it is still a complex organism. The use of embryos did not completely solve the problem of studying cellular effects caused by viruses. Another problem was that bacteria also grow well in embryos, and the effects of viruses often could not be determined accurately in bacterially contaminated embryos.
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