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"+" is able to serve as mRNA. "-" is the complement of +, must function as template to make a complementary strand of + RNA before any translation can occur. Use virus coat morphology. Enveloped vs. non-enveloped viruses. F0 21 2CCjg , c $\PPp   ]Taxonomy of viruses$ H , 0޽h ? ̙33 tlP4(  4 4 s *Ĉu `}  u ZVIROIDS AND PRIONS *H 4 0޽h ? ̙3310 V1N1(0(  (^ ( S $   uH0 ( c $hT$ @  u /F. Life Cycle of Animal Viruses Viruses that infect animal cells replicate by means of what is called the productive life cycle. Some viruses, such as HIV and the herpes viruses are able to become latent in certain cell types. A few viruses increase the risk of certain cancers. We will now look at the life cycles of viruses that infect animal cells. 1. The Productive Life Cycle (def) of Animal Viruses Although there is great variation among the animal viruses, a generalized productive life cycle consists of the following steps: a. Attachment or adsorption Adsorption (def) (see Fig. 1A and Fig. 1B) involves the binding of attachment sites on the viral surface with receptor sites on the host cell cytoplasmic membrane. For a virus to infect a host cell, that cell must have receptors for the virus on its surface and also be capable of supporting viral replication. These host cell receptors are normal surface molecules involved in routine cellular function, but since a portion of a molecule on the viral surface resembles the chemical shape of the body's molecule that would normally bind to the receptor, the virus is able to attach to the host cell's surface. For example, most human rhinoviruses that cause the common cold bind to intercellular adhesion molecules (ICAM-1) found on cells of the nasal epithelium. These ICAM-1 molecules are used normally for the recruitment of leukocytes into the respiratory tract. On the other hand, HIV adsorbs to CD4 molecules and chemokine receptors found on the surface of human T4-lymphocytes and macrophages (discussed later in this section). CD4 molecules are normally involved in immune recognition while chemokine receptors play a role in initiating inflammation and recruiting leukocytes. b. Penetration 1. Enveloped viruses (def) enter the host cell in one of two ways: a. In some cases, the viral envelope may fuse with the host cell cytoplasmic membrane and the nucleocapsid (def) is released into the cytoplasm (see Figs. 2A and Fig. 2B). b. Usually they enter by endocytosis whereby the host cell cytoplasmic membrane invaginates and pinches off, placing the virus in an endocytic vesicle (see Fig. 3A, Fig. 3B, and Fig. 3C). 2. Naked viruses (def) enter the cell in one of two ways: a. In many cases, interaction between the viral capsid and the host cell cytoplasmic membrane causes a rearrangement of capsid proteins allowing the viral nucleic acid to pass through the membrane into the cytoplasm (see Fig. 4A, Fig. 4B, and Fig. 4C). b. The virus may enter by endocytosis whereby the host cell cytoplasmic membrane invaginates and pinches off, placing the virus in an endocytic vesicle (see Fig. 5A, Fig. 5B, and Fig. 5C). c. uncoating Uncoating is the release of the viral genome (def) from the remainder of the virus. 1. With enveloped viruses, the viral envelope is first removed either by fusing with the cytoplasmic membrane during penetration (see Fig. 2B and Fig. 2C) or fusing with the membrane of the endocytic vesicle after endocytosis (see Fig. 7A, Fig. 7B, and Fig. 7C). The viral capsid is then enzymatically removed and the viral genome is released. 2. In the case of naked viruses entering by fusion, interaction between the viral capsid (def) and the host cell cytoplasmic membrane (see Fig. 8) causes a rearrangement of capsid proteins allowing the viral nucleic acid to pass through the membrane into the cytoplasm. With naked viruses entering by endocytosis, the endocytic vesicle and the viral capsid are enzymatically removed and the viral nucleic acid is released into the host cell's cytoplasm (see Fig. 9A, Fig. 9B, and Fig. 9C). Uncoating begins the eclipse period (def), the period during which no intact virions can be detected within the cell. d. Replication The viral genome directs the host cell's metabolic machinery (ribosomes, tRNA, nutrients, energy, enzymes, etc.) to synthesize viral enzymes and viral parts. The viral genome is transcribed into viral mRNA (see Fig. 10) that goes to the host cell's ribosomes where it is translated into viral structural proteins and viral enzymes. (Viral genetics will be discussed in Unit 4.) During the early phase of replication, the viral genome replicates thousands of times. During the late phase of replication, viral structural proteins (capsid and matrix proteins, envelope glycoproteins, etc.) and the enzymes involved in maturation are produced. Also during this time, viral proteins and glycoproteins coded by the viral genome are incorporated into the host cell's membranes (see Fig. 11). During the uncoating and replication stages the virus is not infectious. e. Maturation During maturation, the capsid is assembled around the genome (see Fig. 12A and Fig. 12B). f. Release 1. With naked viruses, the infected cell usually disintegrates and the virions are released (see Fig. 13). 2. With enveloped viruses, the host cell may or may not be lysed. The viruses obtain their envelopes from host cell membranes by budding. As mentioned above, prior to budding, viral proteins and glycoproteins are incorporated into the host cell's membranes. During budding the host cell membrane with incorporated viral proteins and glycoproteins evaginates and pinches off to form the viral envelope. Budding occurs either at the outer cytoplasmic membrane, the nuclear membrane, or at the membranes of the Golgi apparatus. Viruses obtaining their membrane from the cytoplasmic membrane are released during the budding process (see Fig. 14Aand Fig. 14B). Those obtaining their envelopes from the membranes of the nucleus or the Golgi apparatus are then released by exocytosis via transport vesicles (see Fig. 15A and Fig. 15B). Some viruses, capable of causing cell fusion, may be transported from one cell to adjacent cells without being released, that is, they are transmitted by cell-to-cell contact whereby an infected cell fuses with an uninfected cell. g. Reinfection As many as 10,000 to 50,000 animal viruses may be produced by a single infected host cell. KF%%K (j@? 7  ]T  +*6 '>]%@N,4+%  #65:fA B} c   sj     )  T #Z    )  ${  #    ,N  y  O  #q {  fK [  U =|O ;5 2  J   _!0}!0@E!0FR!0W_!0!0!0!0!0p|!0~!0!0!0 !0 !0 !0g s !0u | !0 !0 !0q } !0 !0 !0 !0 !0 !0 !0!0#!0)1!0W\!0!0!0bo!0t}!0!0ly!0}!0%!0*3 !0} !0@E !0FR !0W_ !0 !0 !0 !0  !0p|  !0~  !0  !0  !0  !0  !0  !0g s  !0u |  !0  !0  !0q }  !0  !0  !0  !0  !0  !0  !0 !0# !0)1 !0W\ !0  !0! !0bo" !0t}# !0$ !0ly% !0}& !0%' !0*3H ( 0޽h ? ̙330 06(  0^ 0 S $   u 0 c $\Z$ @  u , D. Classification of Viruses Viruses are often classified by the type of nucleic acid they have for their genome, the shape of their capsid (helical or polyhedral), and whether they are enveloped or naked (lack an envelope). Viruses can store their genetic information in six different types of nucleic acid which are named based on how that nucleic acid eventually forms the viral mRNA (see Fig. 1) able to bind to host cell ribosomes and be translated into viral proteins. These types of nucleic acid are: a. (+/-) double-stranded DNA. The (-) DNA strand is directly transcribed into viral mRNA. Most bacteriophages, Papovaviruses, Adenoviruses, Herpesviruses. b. (+) DNA or (-) DNA. Once inside the host cell, its converted into dsDNA and the (-) DNA strand is transcribed into viral mRNA. Phage M13, Parvoviruses. c. (+) RNA. A (+) RNA is copied into (-) RNA that is transcribed into viral mRNA. Picornaviruses, Togaviruses, Coronaviruses. d. (-) RNA. The (-) RNA is copied into a (+) RNA which functions as viral mRNA. Orthomyxoviruses, Paramyxoviruses, Rhabdoviruses. e. (+/-) double-stranded RNA. The (+) of the (+/-) RNA functions as viral mRNA. Reoviruses. f. (+) RNA. The (+) RNA is reverse transcribed into (-) DNA that makes a complementary copy to become (+/-) DNA. The (-) DNA is transcribed into viral mRNA. Retroviruses. && &Classification of Bacteriophages-the most important criteria are phage morphology and nucleic acid properties A. Morphology 1. Tailless icosahedral 2. Viruses with contractile tails 3. Viruses with noncontractile tails 4. Filamentous viruses B. Nucleic acid properties 1. DNA or RNA 2. Single stranded (ss) or double stranded (ds) x|CO   G1 N LL &g 2[!0!0H 0 0޽h ? ̙33 0   8' (  8^ 8 S $   u  8 c $ $ @  u  E. Viroids and Prions Viroids (def) are even more simple than viruses. They are small, circular, single-stranded molecules of infectious RNA lacking even a protein coat. They are the cause of a few plant diseases such as potato spindle-tuber disease,cucumber pale fruit, citrus exocortis disease, and cadang-cadang (coconuts). Prions (def) are infectious protein particles thought to be responsible for a group of transmissible and/or inherited neurodegenerative diseases including Creutzfeldt-Jakob disease, kuru, and Gerstmann-Straussler- syndrome in humans as well as scrapie in sheep and goats. Most evidence indicates that the infectious prion proteins are modified forms of normal proteins coded for by a host gene in the brain. In the case of the disease scrapie, the normal prion protein in an animal without the disease has alpha-helices in the proteins secondary structure (def) while the scrapie prion protein in diseased animals has beta-sheets for the secondary structure. When the scrapie prion protein contacts the normal protein it causes it to change its configuration to the scrapie beta-sheet form. This suggests that the conversion of a normal prion protein into an infectious prion protein may be catalyzed by the prion protein itself upon entering the brain. Inherited forms may be a result of point mutations that make the prion protein more susceptible to a change in its protein structure. For an article on prions and mad cow disease, see John Brown's "What the Heck is....????" web page. 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