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Color Insert

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Image of COLOR PLATE 1 (Chapter 7)

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COLOR PLATE 1 (Chapter 7)

Echocardiographic features of myocarditis. (A) Two-dimensional parasternal long-axis view demonstrating LV dilation and a pericardial effusion (PE). Color Doppler interrogation provides evidence of mitral regurgitation. (B) Parasternal long-axis view demonstrating LV dilation and normal papillary muscles (P). (C) M mode demonstrating systolic dysfunction with flattened interventricular septal motion (IVS), fair LV posterior wall excursion (LVPW), LV dilation with increased LV end-diastolic dimension (D), and reduced systolic function (S) and PE.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 2 (Chapter 8)

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COLOR PLATE 2 (Chapter 8)

Condyloma acuminatum associated with HPV-6.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 3 (Chapter 8)

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COLOR PLATE 3 (Chapter 8)

Multiple primary squamous cell carcinomas associated with HPV-8 on the forehead of a man with EV.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 4 (Chapter 8)

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COLOR PLATE 4 (Chapter 8)

Disseminated molluscum contagiosum in an AIDS patient.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 5 (Chapter 8)

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COLOR PLATE 5 (Chapter 8)

Nodular stage of orf on the hand of a shepherd from Mexico.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 6 (Chapter 8)

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COLOR PLATE 6 (Chapter 8)

First-episode genital herpes (due to HSV-2) in a man who gave a history of always using condoms during sex.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 7 (Chapter 8)

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COLOR PLATE 7 (Chapter 8)

Recurrent HSV-2 infection of the buttock.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 8 (Chapter 8)

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COLOR PLATE 8 (Chapter 8)

Herpes whitlow due to HSV-2 in a health care worker following a puncture wound from a needle used to culture genital herpes.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 9 (Chapter 8)

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COLOR PLATE 9 (Chapter 8)

Erythema multiforme following an outbreak of herpes labialis.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 10 (Chapter 8)

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COLOR PLATE 10 (Chapter 8)

Primary varicella in an adult Japanese man.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 11 (Chapter 8)

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COLOR PLATE 11 (Chapter 8)

Thoracic herpes zoster in an otherwise healthy man.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 12 (Chapter 8)

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COLOR PLATE 12 (Chapter 8)

Oral hairy leukoplakia associated with EBV in an AIDS patient.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 13 (Chapter 8)

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COLOR PLATE 13 (Chapter 8)

Papules of Gianotti-Crosti syndrome associated with EBV.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 14 (Chapter 8)

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COLOR PLATE 14 (Chapter 8)

Kaposi’s sarcoma associated with HHV-8 in an HIV-negative elderly Italian man.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 15 (Chapter 8)

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COLOR PLATE 15 (Chapter 8)

Erythema infectiosum (fifth disease) associated with parvovirus B19.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 16 (Chapter 8)

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COLOR PLATE 16 (Chapter 8)

Measles in an infant.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 17 (Chapter 8)

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COLOR PLATE 17 (Chapter 8)

Bacillary angiomatosis associated with in an HIV-positive man.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 18 (Chapter 10)

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COLOR PLATE 18 (Chapter 10)

Intense papillary response in the superior conjunctival tarsal plate due to adenovirus infection. (Reprinted from N. K. Ragge and D. L. Easty, ed., , Mosby Year Book, Inc., Philadelphia, PA, 1991, with permission of Elsevier.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 19 (Chapter 10)

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COLOR PLATE 19 (Chapter 10)

Acute hemorrhagic conjunctivitis. (Courtesy of P. Asbell. Reprinted from N. K. Ragge and D. L. Easty, ed., Mosby Year Book, Inc., Philadelphia, PA, 1991, with permission of Elsevier.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 20 (Chapter 10)

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COLOR PLATE 20 (Chapter 10)

Large ameboid corneal ulcer in a malnourished child with measles. (Courtesy of J. Stanford Smith. Reprinted from N. K. Ragge and D. L. Easty, ed., , Mosby Year Book, Inc., Philadelphia, PA, 1991, with permission of Elsevier.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 21 (Chapter 10)

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COLOR PLATE 21 (Chapter 10)

Dendritic corneal ulceration demonstrated using fluorescein and illuminated in cobalt blue light.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 22 (Chapter 10)

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COLOR PLATE 22 (Chapter 10)

Ameboid corneal ulceration occurring as a result of locally induced immunosuppression by steroids. Both Rose Bengal and fluorescein stains were used.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 23 (Chapter 10)

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COLOR PLATE 23 (Chapter 10)

Diffuse scleritis secondary to herpes zoster. Note the dusky red color due to the injection of the scleral, episcleral, and conjunctival vascular beds.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 24 (Chapter 10)

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COLOR PLATE 24 (Chapter 10)

CMV optic neuritis. Note the clear view indicative of little vitreous inflammation. (Courtesy of S. Lightman.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 25 (Chapter 14)

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COLOR PLATE 25 (Chapter 14)

Three-dimensional structure of the interaction of influenza virus HA with a neutralizing antibody. (A) α-Carbon backbone structure of a water-soluble influenza virus HA released from viral membranes by protease digestion, as determined by X-ray crystallography (57, 58). Individual subunits of the trimeric structure are colored red, blue, and yellow. The molecule is oriented such that the sialic acid binding pockets are at the top and the region that connects with the membrane anchor domain is toward the bottom. (B) α-Carbon backbone structure of the variable domain of an anti-HA MAb. The heavy and light chains, respectively, are dark and light blue. The molecule is oriented with the antigen-binding region toward the top. (C) Interaction of HA with the variable region of an anti-HA MAb (3). Antibody colors are the same as in panel B; HA is in red. The region of the HA bound by the MAb is located in panel A by the arrow. (D) Top view of HA trimers, looking toward the membrane surface. The side chain of the single modified residue in an antigenic MAb escape variant (selected by a different antibody than those shown in panel C or D) is in white. Note the exposed location. Comparison of variant and wild-type structures revealed only minimal conformational alterations: the new side chain simply replaces its predecessor.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 26 (Chapter 14)

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COLOR PLATE 26 (Chapter 14)

Three-dimensional structure of MHC class I and class II molecules. Shown is the structure of the α-carbon backbone of class I (left) and class II (right) molecules (48) bearing antigenic peptides (short red ribbon) in the groove, as determined by X-ray crystallography of water-soluble molecules released from the cell surface by protease digestion. The molecule is oriented with the top toward the TCR.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 27 (Chapter 14)

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COLOR PLATE 27 (Chapter 14)

Three-dimensional structure of MHC molecules bearing antigenic peptides. Ribbon α-carbon backbone (top) and space-filling main- and side-chain (bottom) representations of class I (9, 46) (left) and class II (right) molecules bearing antigenic peptides from viral proteins. The view is from the perspective of a TCR.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 28 (Chapter 14)

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COLOR PLATE 28 (Chapter 14)

Time course of an idealized antiviral immune response. (A) Response to a primary viral infection. All values are in arbitrary activity units, except the magnitude of serum Ig responses, which is expressed in relative amounts of protein. Since IgG antibodies are of higher affinity than IgM antibodies, the IgG response will have a much greater biological effect on viral replication. “T cells” represents the aggregate activities of T and T (B) Response to a secondary viral infection. Note that the presence of preexisting antibodies limits (or sometimes completely prevents) the replication of viruses serologically cross-reactive to those previously encountered. The presence of a cross-reactive antigen triggers a rapid increase in IgG antibodies. T-cell responses occur more rapidly but may not include T if viral replication is greatly limited. The reduction in IFN and NK cell activity merely reflects the decreased number of virus-infected cells.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 29 (Chapter 18)

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COLOR PLATE 29 (Chapter 18)

Schematic representation of the genome of the WR strain of VACV. The genome is a linear double-stranded molecule with terminal hairpins, inverted terminal repeats, and a series of direct repeats within the inverted repeats. Each overlapping bar indicates gene conservation between the WR strain and all poxviruses, vertebrate poxviruses, and orthopoxviruses. The bars are color coded according to the percentage of gene conservation across the indicated taxa. (Reprinted from reference 15 with permission.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 30 (Chapter 21)

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COLOR PLATE 30 (Chapter 21)

The V2V genome. The 125-kbp linear double-stranded DNA consists of a long unique segment (U) of approximately 100 kbp that is flanked by terminal and internal repeats of 88 bp (TR and IR) and a short unique sequence (U) of approximately 5.4 kbp that is bounded by repeated sequences (TR and IR) of 6.8 kbp. There are two origins (ori) for DNA replication in the repeats that bound the U. ORFs are to scale and are identified by number; genes containing ORFs below the genome are transcribed from right to left, while those above the genome are transcribed from left to right. Red is used for the ORFs for IE genes, green is used for glycoproteins, and blue is used for DNA synthesis and nucleotide metabolism. ORFs 62, 63, and 64 are present in two copies, as they are fully contained within the repeats flanking the U.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 31 (Chapter 22)

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COLOR PLATE 31 (Chapter 22)

Consensus genetic map of wild-type HCMV based on the Merlin genome. RL and RS (which contain the sequence as a direct repeat at the genome termini and as an inverted repeat internally) are shown in a thicker format than UL and US. Protein-coding regions are indicated by colored arrows grouped according to the key, with gene nomenclature below. Introns are shown as narrow white bars. Genes corresponding to those in AD169 RL and RS are given their full nomenclature, but the UL and US prefixes have been omitted from UL1-UL150 (12 to 194 kbp) and US1-US34A (199 to 231 kbp). Colors differentiate between genes on the basis of conservation across the and (core genes) or between the - and (subcore genes), with subsets of the remaining noncore genes grouped into gene families. GPCR, G-protein-coupled receptor. (Reprinted from reference 46 with permission.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 32 (Chapter 25)

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COLOR PLATE 32 (Chapter 25)

Map of KS prevalence throughout Africa prior to the AIDS epidemic. This map was constructed from surveys performed by Denis Burkitt, who first described Burkitt’s lymphoma. It is evident that KS was hyperendemic throughout this continent. With the onset of the AIDS epidemic, a second epidemic of KSHV-related cancer has occurred, and KS is the most commonly reported cancer in most sub-Saharan African countries.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 33 (Chapter 26)

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COLOR PLATE 33 (Chapter 26)

Adenoviral tonsillitis in a 3-year-old child. Note the follicular exudates. (Reprinted from reference 114 with permission.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 34 (Chapter 28)

Plantar wart, myrmecia. (Courtesy of Mark H. Goldgeier, University of Rochester.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 35 (Chapter 28)

Common wart. (Courtesy of Mark H. Goldgeier, University of Rochester.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 36 (Chapter 28)

Plantar wart, mosaic wart. (Courtesy of Mark H. Goldgeier, University of Rochester.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 37 (Chapter 28)

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COLOR PLATE 37 (Chapter 28)

Warty keratosis on the forearm of a transplant recipient. (Courtesy of Anthony A. Gaspari, University of Maryland.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 38 (Chapter 28)

Epidermodysplasia verruciformis, pityriasis-like plaques caused by HPV. (Courtesy of Eliott J. Androphy, University of Massachusetts.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 39 (Chapter 28)

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COLOR PLATE 39 (Chapter 28)

Condylomata acuminata of the penis. Lesions are at different stages of development.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 40 (Chapter 28)

Large pigmented condyloma acuminatum of the inguinal fold. The clinical appearance is also consistent with bowenoid papillomatosis.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 41 (Chapter 28)

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COLOR PLATE 41 (Chapter 28)

Colpophotograph showing a well-developed cervical condyloma adjacent to a flat, pale acetowhite area (upper quadrants of the cervix) with jagged borders and satellite lesions, consistent with a low-grade HPV infection. (Courtesy of Richard C. Cherkis, University of Rochester.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 42 (Chapter 28)

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COLOR PLATE 42 (Chapter 28)

Colpophotograph demonstrating different grades of HPV cervical disease. Centered around the cervical os is an acetowhite area with an internal gray-white demarcation and a few punctate vessels suggestive of a moderate-grade lesion. This lesion is surrounded, mostly in the lower quadrants, by a fainter acetowhite area, with straight margins and no vessels suggestive of a lower-grade HPV lesion. (Courtesy of Richard C. Cherkis, University of Rochester.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 43 (Chapter 28)

Buschke-Loewenstein tumor of the inguinal fold.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 44 (Chapter 28)

Laryngeal papilloma narrowing the airway. (Courtesy of Haskins K. Kashima, Johns Hopkins University.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 45 (Chapter 35)

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COLOR PLATE 45 (Chapter 35)

Computer image reconstruction of a rotavirus TLP based on cryoelectron microscopy. The diameter of the viral particle, including the spikes, is 1,000 Å. Both the outer and inner capsids are constructed with a T = 131 (levo) icosahedral lattice symmetry. VP4 (the spike protein) and VP7 compose the outer viral layer; in the cutaway, the middle layer is composed of VP6, and inside this layer can be seen the core (that surrounds VP1 and VP3 and the viral RNA) formed by VP2. (Image courtesy of Mark Yeager, reproduced with permission from reference 155.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 46 (Chapter 37)

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COLOR PLATE 46 (Chapter 37)

Koplik’s spots on the oral mucosa of a child with measles seen just after the appearance of the rash. The erythematous mucosa is peppered with numerous tiny bluish-white elevations. (Courtesy of the late Saul Krugman.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 47 (Chapter 39)

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COLOR PLATE 47 (Chapter 39)

NiV infection in the brain of a person for whom the infection was fatal. Viral antigens are present in neurons and neuronal processes. Immunoalkaline phosphatase staining, naphthol fast red substrate with light hematoxylin counterstain; original magnification, ×100. (Photomicrograph courtesy of S. R. Zaki and W. J. Shieh.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 48 (Chapter 40)

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COLOR PLATE 48 (Chapter 40)

Map of human rabies deaths in 2003. (Source: World Health Organization [http://gamapserver.who.int/mapLibrary/app/searchResults.aspx].)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 49 (Chapter 40)

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COLOR PLATE 49 (Chapter 40)

Concentric spread of raccoon rabies in the eastern United States between 1977 and 1993. (Reprinted from reference 31a with permission.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 50 (Chapter 40)

Distribution of terrestrial rabies strains in the United States in 2006. (Reprinted from reference 16.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 51 (Chapter 40)

Immunofluorescence staining of rabies antigen in brain tissue.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 52 (Chapter 40)

Clinical features of furious rabies. (A) The grimace and stare which accompany the pharyngeal spasms of hydrophobia. (B) Aerophobia provoked by air movement across the patient’s face. (C) Inspiratory spasm. (Reprinted from reference 78a with permission of .)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 53 (Chapter 45)

Newborn with overwhelming sepsis due to echovirus 11. Note typical EV exanthem. This child’s illness began within the first week of life and ended with her death due to hepatic failure at approximately 1 month of age.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 54 (Chapter 48)

Structure of Norwalk virus (NV) particles. (a) Surface representation of the three-dimensional surface structure of recombinant NV (rNV) particles viewed along the icosahedral threefold axis. This structure was determined by image processing of the rNV particles shown in Fig. 1C. The rNV particles have a distinct architecture, and they exhibit T=3 icosahedral symmetry; the twofold, threefold, and fivefold axes of symmetry are shown. Cup-like depressions are evident at the threefold and fivefold axes. The capsid structure is made up of 90 arch-like dimers of a single protein that form two types of capsomers; A/B capsomers ( = 60) surround the three- and fivefold axes of symmetry, and C/C capsomers ( = 30) are located at the twofold axes of symmetry. (b) Summary of the properties of the single protein that makes up the NV capsid structure. A linear schematic of the three domains (C, conserved; V, variable; LC, less conserved) in the single capsid protein and a region predicted to fold into an eight-stranded antiparallel beta-barrel is shown. (c) X-ray crystallographic structure of rNV capsid at 3.4-Å resolution, as viewed along the icosahedral twofold axis. Only backbone atoms of the 180 subunits are depicted, and the structure is depth cued, with deeper blue at lower radii and lighter blue at higher radii. (d) Ribbon presentation of the C subunit of rNV capsid protein. The N-terminal arm, S domain, and P1 and P2 subdomains are colored in green, yellow, red, and blue, respectively. The N and C termini of the capsid protein are indicated. The C terminus faces a hollow, the N terminus faces the interior of the capsid, and the P2 subdomain faces the exterior of the capsid. (Panels a, c, and d kindly provided by B. V. V. Prasad; modified from references 105a and 106 with permission.)

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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Image of COLOR PLATE 55 (Chapter 57)

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COLOR PLATE 55 (Chapter 57)

Inflamed mammary glands of scrapie-infected sheep accumulate PrP. (Top) Western blots with a PrP-specific antibody. Lanes 1 to 3, 9 to 11, and 14 to 16 from left: native and PK-digested brain homogenates (diluted 1,400-fold) from a scrapie-infected (Scr) and a scrapie-free (Scr) sheep. Lanes 6 to 8: mammary glands from an Scr sheep with follicular mastitis (mast), an Scr sheep from a flock with neither visna/maedi virus seropositivity nor mastitis (mast), and an Scr mast sheep. Each one of five Scr mast sheep displayed mammary PrP (lanes 4, 5, 12, 13, and 17). Non-scrapie-infected brain and mammary gland extracts showed no PrP upon PK digestion (lanes 3, 6 to 8, 11, and 16). (Middle) Mammary gland micrographs from visna/maedi virus-seropositive Scr mast sheep and from Scr mast sheep. Lymphoid follicles are adjacent to milk ducts (md). Immunofluorescence stains reveal abundant PrP deposits within mammary lymphoid follicles (arrow) from Scr but not from Scr sheep. GC, germinal center (the area including FDCs). (Bottom) PK-treated paraffin-embedded tissue (PET) blots of mammary gland sections reveal punctate PrP deposits colocalizing with lymphoid follicles in Scr mast but not in Scr mast sheep. HE, hematoxylin and eosin.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 56 (Chapter 57)

Mammary PrP localizes to macrophages and FDCs. (Top) Mammary gland from a sheep with coincident mastitis, visna/maedi virus seropositivity, and scrapie (sample no. 732). Shown are confocal laser scanning micrographs of lymphoid follicles immunostained for PrP (green), macrophages (Mφ, red) or FDCs (red), and nuclear DNA (blue). PrP associates with CD68 Mφ and FDCs in scrapie-positive (Scr, arrows) but not in scrapie-free (Scr) sheep. Bars = 6.3 µm (top) and 7.5 µm (bottom). (Bottom) CD68 macrophages (arrow) and degenerating leukocytes within milk ducts and in adjacent lymphoid follicles of an inflamed mammary gland, as well as in milk sediment (inset, arrowheads). Bars = 100 µm (mammary gland) and 20 µm (milk cells).

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 57 (Chapter 57)

Induction of tertiary follicles and prion replication competence in nonlymphoid organs. (A) Hypothetical hierarchical cascade inducing the generation of tertiary follicles in nonlymphoid organs, and possibly giving rise to ectopic prion replication competence. Autoimmune diseases as well as chronic lymphocytic inflammations have been demonstrated to induce prion replication competence in nonlymphoid organs (green), whereas others have not been investigated yet (question marks). (B) Schematic drawing of the events that contribute to the generation of tertiary follicles upon an inflammatory stimulus that has attracted and activated lymphocytes and induced up-regulation of LTs. LTβR stromal precursor cells will be activated upon binding to LTs (LTα or LTαβ) provided by lymphocytes, leading to the expression of homeostatic chemokines and further LTs, generating a positive-feedback loop that leads to the formation of tertiary follicles containing FDCs and other cells of the immune system.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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COLOR PLATE 58 (Chapter 57)

Histologic features of prion diseases. CNS parenchyma of sCJD (A and B) and vCJD (C and D) showing astrogliosis and widespread spongiform changes. PrP depositions are synaptic (A and B) and in the form of florid plaques (asterisks [C and D]). Panels A and C are standard hematoxylin-eosin stains; panels B and D are immunohistochemical stainings for PrP. Bars = 50 µm.

Citation: Richman D, Whitley R, Hayden F. 2009. Color Insert, In Clinical Virology, Third Edition. ASM Press, Washington, DC.
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