Media For Multiplitoplasma Viroids Is Not Rare

Viral proteins that are to become spikes of virus attach to host plasma membrane.

Viral matrix protein coats inside of plasma membrane.

Viral matrix protein coats inside of plasma membrane.

Matrix protein

Nucleocapsid becomes enclosed by viral envelope which is composed of the host's plasma membrane (shown in green)

Matrix protein

Nucleocapsid becomes enclosed by viral envelope which is composed of the host's plasma membrane (shown in green)

Figure 14.11 Mechanism for Releasing Enveloped Virions (a) Process of budding. (b) Electron micrograph of virus particles budding from the surface of a human cell.The virion on the left has completed the process.The other three are in various degrees of completion. It is clear from the micrograph how the virions gain the plasma membrane of the host cell. Note that the membrane of the host remains intact after budding has been completed.

100 nm

Figure 14.11 Mechanism for Releasing Enveloped Virions (a) Process of budding. (b) Electron micrograph of virus particles budding from the surface of a human cell.The virion on the left has completed the process.The other three are in various degrees of completion. It is clear from the micrograph how the virions gain the plasma membrane of the host cell. Note that the membrane of the host remains intact after budding has been completed.

largely by whether a virus can be detected in the body during the long period of persistence (figure 14.12).

A persistent infection may or may not cause disease, but since the infected person carries the virus, he or she is a potential source of infection to others. In all cases, the person is a carrier and therefore able to spread disease. Some persistent infections have features of more than one of these categories. These depend on such circumstances as the time after infection and the cell type in which the virus is located. For example, infection by HIV has features of latent, chronic, and slow infections.

Late Complications that Follow an Acute Infection

An example of a late complication that follows an acute infection is subacute sclerosing panencephalitis (SSPE), which follows an acute measles infection (see figure 14.12a). This invariably fatal brain disorder occurs in about one in 300,000 people up to 10 years after a person has had measles.

100 nm

Table 14.6 Comparison of Replication Cycle of Bacteriophages and Animal Viruses in Virulent Infections

Stage

Bacteriophages

Animal Viruses

Attachment

Fusion of capsid with host membrane does not occur.

Fusion of viral envelope and host membrane common.

Entry

Only nucleic acid enters cell—no enzymes.

Entire virion enters cell, including enzymes of replication.

Targeting of virion

Targeting unnecessary

Targeting to site of viral replication.

Uncoating

Takes place at surface of cell

Takes place inside the cell

Replication cycle

Depends on whether nucleic acid is DNA or RNA, double-or single-stranded.

Same pattern of replication as phage with the same genome.

Exit

In lytic infection, phage codes for lytic enzyme, which lyses the cell. Budding rare—cells not killed.

Cell dies and lyses with release of virus. Budding common— cells may or may not be killed.

Nester-Anderson-Roberts: I II. The Microbial World I 14. Viruses, Prions, and I I © The McGraw-Hill

Microbiology, A Human Viroids: Infectious Agents Companies, 2003

Perspective, Fourth Edition of Animals and Plants

Measles

354 Chapter 14 Viruses, Prions, and Viroids: Infectious Agents of Animals and Plants

Latent Infections

Latent infections are those in which an acute infection is followed by a symptomless period and then reactivation of the disease occurs. Infectious virus particles cannot be detected until the disease is reactivated (see figure 14.12b). The symptoms of the initial and reactivated forms of the disease may differ. The viruses causing latent infections can be either DNA or RNA viruses. The best known examples are caused by members of the her-pesvirus family (Herpesviridae), which is divided into two herpes simplex types: HSV-1 and HSV-2. The latter, frequently called genital herpes, is an important and common sexually transmitted disease. ■ HSV-1, p. 607 ■ HSV-2, p. 607

Initial infection of young children with herpes simplex type 1 (HSV-1) may not lead to any symptoms, but cold sores and fever blisters often result. After this initial acute infection, the HSV-1 infects the sensory nerve cells, where it remains in a non-infectious form without causing symptoms of disease (figure 14.13). Replication of this virus in the nerve cells is repressed by some unknown mechanism but can be activated by such conditions as menstruation, fever, or sunburn. Following the start of replication, mature infectious virions are produced and are carried to the skin or mucous membranes by the nerve cells, once again resulting in cold sores. After these sores have healed, the virus and host cells once again exist in harmony and, as with other latent infections, no virions are synthesized until the disease recurs. ■ herpes simplex type 1,p. 607 Another example of a latent infection is provided by another member of the herpesvirus family, varicella-zoster virus, the cause of chickenpox (varicella). Initial infection of normal children results in a rash termed chickenpox. This virus can remain latent for years without producing any disease symptoms. It can then be reactivated and produce the disease called shingles, or herpes zoster. Thus, chicken pox and shingles are different diseases caused by the same virus. Most infections, however, never reactivate. ■ chicken-pox, p. 546 ■ shingles, p. 548

Most herpesviruses, including HSV-2, tend to become latent under various conditions. It appears that part or all of the viral DNA becomes integrated into the genome of the host, or copies of the nucleic acid of some herpesviruses may replicate as plasmids in the host cell. Note the similarity to infection by temperate phages. Table 14.7 gives some examples of latent infections. ■ temperate phages, p. 329 ■ plasmids, p. 209

HIV infection

Figure 14.12 Time Course of Appearance of Disease Symptoms and Infectious Virions in Various Kinds of Viral Infections

Chronic Infections

In chronic infections, the infectious virus can be demonstrated at all times (see figure 14.12c). Disease may be present or absent during an extended period of time or may develop late. The best known chronic human infection is caused by the hepatitis B virus, formerly called serum hepatitis virus. This disease is transmitted sexually or from the blood of a chronic carrier who shows no symptoms. Some people who contract the virus develop an acute illness marked by nausea, fever, and jaundice. About 300 million people are carriers of the virus, and a significant number develop cirrhosis or cancer of the liver; more than 1 million people die each year from hepatitis B. ■ hepatitis B, p. 621

In the carrier state, infectious virions of hepatitis B are continually produced and can be detected in the bloodstream, saliva, and semen. The viral DNA genome may also occur as a plasmid in liver cells (hepatocytes), where it replicates and produces many infectious virions. Following replication in this plasmid state, the genome can also integrate into the cells of the liver. In this state, only some of the protein components of the virion are synthesized

Infectious virus

Disease

Acute infection with late complications

(measles- Subacute Sclerosing Panencephalitis [SSPE])

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