Chapter 19 : Poxviruses

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Smallpox has long been known as a severe human disease (1, 2) and was already endemic in India 2,000 years ago before spreading to China and Japan in the east and Europe and North Africa in the West by about 700 A.D. It was introduced to the Caribbean with the African slave trade in 1518 and thence to Mexico in 1520, taking a terrible toll on the totally nonimmune Amerindians. Repeated introductions from Europe and, to a lesser extent, from Africa, into North America occurred from 1617 onward. With the discovery of vaccination by Jenner in the latter part of the 18th century (3), the disease was brought under control first by local initiatives, which became national, and finally global. Following the last identified case in 1977, the world was certified free of smallpox by the World Health Assembly in May 1980 (2). The subsequent drawdown of vaccine stockpiles and cessation of childhood vaccination programs have increased the vulnerability of the human population to a devastating smallpox epidemic and increased the threat of variola virus (VARV) as a bioweapon. This unintended consequence of the most successful vaccination program in history was exploited by the former Soviet Union, which weaponized VARV in contradiction to the 1972 Biological and Toxin Weapons Convention (4, 5). This occurrence raised concerns that other rogue nations or terrorist groups could also develop VARV or monkeypox virus (MPXV) as a bioweapon.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 1

Structure of virions of poxviruses that cause human infections. Shown are negatively stained preparations of orthopoxvirus virions (cowpox, monkeypox, vaccinia, and variola viruses) (A), parapoxvirus virions (ORFV, BPSV, PCPV, and sealpox viruses) (B), and yatapoxvirus virions (TANV and YMTV) (C). The virions of orthopoxviruses and yatapoxviruses have similar morphologies, but those of yatapoxviruses always have two membranes. Virions of the parapoxviruses are smaller and have a distinctive regular-surface structure. (D) Diagram of the structure of the virion of VACV. The viral DNA and several proteins within the core are organized as a nucleosome. The core has a 9-nm-thick shell with a regular subunit structure. Within the virion, the core assumes the shape of a dumbbell because of the large lateral bodies, which are, in turn, enclosed within a protein shell about 12 nm thick—the first membrane, the surface of which appears to consist of irregularly arranged surface tubules, which, in turn, consist of small globular subunits. Mature virus released by exocytosis (extracellular virus) is enclosed within a second membrane (envelope) acquired from the Golgi. This membrane contains host-cell lipids and several unique virus-specific polypeptides not found in the intracellular mature virus outer membrane. Most virions remain cell-associated and are released by cellular disruption, without the second membrane. (E) Diagram of the structure of the virion of ORFV. The first membrane consists of a single long tubule that appears to be wound around the particle. In negatively stained preparations (B) both sides are visible, giving a characteristic criss-cross appearance. The second membrane is usually closely applied to the surface of the first membrane. Bar = 100 nm.

Reprinted from reference ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 2

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 ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 3

Diagram illustrating the replication cycle of vaccinia virus, the prototype orthopoxvirus. IV, immature virus; MV, mature virus; WV, wrapped virus; EV, extracellular virus.

Reprinted from reference ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 4

Diagram illustrating the epidemiology of cowpox and buffalopox. Solid lines represent known paths of transmission; broken lines represent presumed or possible paths of transmission. (A) Identified wild-rodent reservoir hosts of cowpox include bank voles, wood mice, and short-tailed voles in Great Britain and probably elsewhere in Europe; lemmings in Norway; and susliks and gerbils in Turkmenistan. The traditional liaison hosts from which humans were infected were cows, but currently the most common liaison hosts are domestic cats. White rats, the source of disastrous outbreaks in animals in the Moscow Zoo in 1973 and 1974 ( ), probably acquired infection from wild-rodent-contaminated straw or other bedding material. (B) In India, Egypt, and Indonesia, in the days of smallpox vaccination, buffaloes were sometimes infected with vaccinia virus from recently vaccinated humans, causing what was called buffalopox. Buffalopox seems to have disappeared in Indonesia and Egypt but is still a problem in several states of India. Since the cessation of vaccination, infected buffaloes constitute a source of infection of humans. It is possible that the virus can be maintained by serial transmission in buffaloes, but on the analogy of cowpox in Europe, it is possible that there is an unknown rodent reservoir.

Reprinted from reference ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 5

Diagrammatic representation of the mode of spread of ectromelia virus through the body in mousepox.

Reprinted from reference ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 6

Intracellular inclusions (Guarnieri bodies) in a biopsy from a patient from Somalia prior to smallpox eradication.

Courtesy of Dr. Dirk Elston.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 7

Section of a skin lesion of molluscum contagiosum.

Courtesy of CDC/ Dr. Edwin P. Ewing, Jr., Public Image Library ID# 860.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 8

Clinical features of smallpox and monkeypox. (Left) The rash of smallpox in a boy in Bangladesh in 1974. (Middle) Rear view of a 7-year-old girl from Zaire with monkeypox, on the eighth day after the appearance of the rash. Note the enlargement of the cervical lymph nodes, a feature not seen in smallpox. (Right) Another example of lymphadenopathy associated with monkeypox infection.

Courtesy of CDC/Jean Roy, Public Image Library ID# 10654.

Reprinted from reference ( ) with permission.

Courtesy of CDC/Brian W. J. Mahy, Public Image Library #12778.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 9

Localized zoonotic infections with poxviruses. (A and B) Lesions on hands acquired by milking infected cows: cowpox, caused by an orthopoxvirus (A), and milker's nodes, caused by a parapoxvirus, PCPV (B). (C) Parapoxvirus lesion of ORFV, acquired by handling sheep or goats suffering from contagious pustular dermatitis. (D) Lesion of tanapox on an arm of a child in the DRC. The virus was transmitted mechanically by mosquitoes from an animal reservoir host.

Panels A and B courtesy of D. Baxby; panel C courtesy of J. Nagington; panel D courtesy of Z. Jezek.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 10

Smallpox vaccination. (Left) Tip of a bifurcated needle used to vaccinate individuals containing some vaccine solution. (Right) Primary response to vaccination; typical vesiculo-pustular response.

Courtesy of CDC, Public Image Library ID# 2667.

Courtesy of CDC/Arthur E. Kaye, Public Image Library ID# 3238.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 11

Molluscum contagiosum lesions. (Left) 9-year-old boy with multiple skin-colored molluscum papules on his face and neck. Reprinted from reference ( ) with permission. (Right) Molluscum in a 33-year-old man with AIDS.

Reprinted from reference ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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Image of FIGURE 12

Severe complications of vaccination. (A) Eczema vaccinatum in an unvaccinated sibling of a vaccinated individual. (B) Progressive vaccinia (vaccinia gangrenosum), which was fatal in a child with a congenital defect in cell-mediated immunity. (C) Generalized vaccinia, 10 days after primary vaccination; benign course, no scarring. (D) Ocular vaccinia after autoinoculation.

Reprinted from reference ( ) with permission.

Citation: Isaacs S, Buller R. 2017. Poxviruses, p 387-413. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch19
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