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Chapter 43 : : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses

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Abstract:

The family is the largest family of animal viruses and includes many viruses that are known human pathogens. The clinical diseases produced in humans range from acute febrile illnesses, such as sandfly fever, to more distinct clinical syndromes such as California encephalitis (CE), Rift Valley fever (RVF), Crimean-Congo hemorrhagic fever (CCHF), hemorrhagic fever with renal syndrome (HFRS), and the recently recognized hantavirus cardiopulmonary syndrome (HCPS), which is also referred to as hantavirus pulmonary syndrome. Representative groups and complexes for the bunyaviruses, phleboviruses, and nairoviruses, including major human pathogens, are discussed. The limited host range and similar phylogenetic relationships among hantaviruses and among the rodent hosts have led to the suggestion that hantaviruses may have coevolved with their rodent hosts. Although infection with the hantaviruses causing HFRS occurs in all age groups, infection and disease peak in adults 15 to 40 years of age; like HCPS, HFRS is uncommon in children. The role of viremia in the pathogenesis of HFRS and HCPS is not known, but there is emerging evidence that viremia with ANDV routinely precedes the onset of symptoms and development of antihantavirus antibodies in HCPS by periods of up to 15 days. In eastern Asia, infection with Hantaan and Seoul hantaviruses is usually diagnosed serologically with immunofluorescence assay (IFA), enzyme-linked immunosorbent assay (ELISA), or bead agglutination formats, and IgM antibody is determined by IgM capture ELISA. Investigational strategies include DNA vaccination for pathogenic hantaviruses, including Hantaan virus and ADNV.

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43

Key Concept Ranking

Rocky Mountain Spotted Fever
0.44476148
Acute Respiratory Distress Syndrome
0.44476148
Rocky Mountain Spotted Fever
0.44476148
Hemorrhagic Fever With Renal Syndrome
0.43344727
Sin nombre virus
0.41615048
0.44476148
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Figures

Image of FIGURE 1
FIGURE 1

Model for replication of The principal steps in replication are as follows: 1, attachment, in which G1 and/or G2 proteins bind to an unidentified receptor; 2, entry and uncoating, probably mediated by fusion; 3, replication, cRNA synthesis from vRNA genome; 4, transcription, mRNA synthesis from vRNA genome; 5, replication, vRNA synthesis from the cRNA template; 6, translation, L and M mRNA translation on free ribosomes and M translation on rough endoplasmic reticulum; 7, transport, movement of L, M, and S genomes into the Golgi complex and RDRP and N proteins; 8, packaging, assembly of genomic RNAs and proteins at the Golgi apparatus; 9 and 10, budding and transport, in which Golgi vesicles carry virions to the plasma membrane (PM); 11, fusion and virion release. (Courtesy of C. Jonsson, Department of Molecular Biology, Southern Research Institute.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 2
FIGURE 2

Distribution of and location of hantavirus pulmonary syndrome cases as of 9 May 2006. The total number of cases was 438 in 30 states. (From the CDC.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 3
FIGURE 3

Worldwide distribution of CCHF virus. (Reprinted from reference with permission of Elsevier.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 4
FIGURE 4

Peripheral blood smear from a patient with the cardiopulmonary stage of HCPS. Note the immunoblast with basophilic cytoplasm, prominent nucleolus, and high nuclear-to-cytoplasmic ratio. Also note immature neutrophils. (Courtesy of R. Fedderson.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 5
FIGURE 5

Pulmonary histology in a patient who died from HCPS. Note the intra-alveolar and septal edema, interstitial infiltrates with mononuclear cells, and sparse hyaline membrane. In contrast to patients with acute respiratory distress syndrome, the hyaline membranes are largely devoid of inflammatory cells and cellular debris. (Courtesy of K. Nolte.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 6
FIGURE 6

Clinical course and typical laboratory findings in severe HCPS and severe HFRS. (Reprinted from reference with permission.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 7
FIGURE 7

Bilateral pulmonary edema in a patient with the cardiopulmonary stage of HCPS. (Courtesy of L. Ketai.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 8
FIGURE 8

Flow diagram for the management of patients suspected of having HCPS in the cardiopulmonary stage pending IgG and IgM antihantavirus antibody results. Potential exposure at any time during the 6 weeks before the onset of symptoms includes living in or visiting any area, usually rural, where a rodent reservoir of a pathogenic hantavirus may be present or close contact with a person with HCPS who could have acquired ANDV infection. (Reprinted from reference with permission.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 9
FIGURE 9

Clinical and laboratory course of CCHF. (Reprinted from reference with permission of Elsevier.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 10
FIGURE 10

Serologic results in 66 patients with CE. The geometric means are plotted for neutralizing (Nt), HI, and CF titers, and the arithmetic means are plotted for precipitin antibodies. (Reprinted from reference with permission.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 11
FIGURE 11

SNV recombinant Western blot assay for HCPS. Each panel is a replicate Western blot that contains SNV N (N) and SNV G1 (G1) proteins in separate lanes. The first two panels were reacted with serum from a patient with a clinical syndrome consistent with HCPS. Separate blots were used to detect IgG antibodies (first panel) and IgM antibodies (second panel). The serum sample was found to contain strong IgG and IgM reactivities to SNV N, strong IgG reactivity to SNV G1, and weak IgM reactivity to SNV G1. This pattern is typically seen for patients presenting with acute HCPS. Positive and negative serum samples, respectively, were tested with the blots shown in the last two panels. (Reprinted from reference with permission.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 12
FIGURE 12

Survival without ECMO among ribavirin recipients versus placebo recipients in a trial of intravenous ribavirin therapy for HCPS. Solid line, ribavirin recipients ( = 10); broken line, placebo recipients ( = 13). (Reprinted from reference with permission.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Image of FIGURE 13
FIGURE 13

Effect of ribavirin or placebo therapy on patients with serologically confirmed HFRS. Top, percent mortality by enrollment date. Bottom, survival and death by study year. From the drug effect model the odds of death in controls were estimated as seven times greater than in the ribavirin group (95% confidence interval, 1.2 to 39.9). Baseline covariates in the logistic regression model were total serum protein and aspartate aminotransferase. (Reprinted from reference with permission of The University of Chicago Press.)

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
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Tables

Generic image for table
TABLE 1

genera, subgroups, and selected viruses that are human pathogens, excluding hantaviruses

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
Generic image for table
TABLE 2

Hantavirus species recognized to date

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
Generic image for table
TABLE 3

Natural vertebrate hosts, vectors, and mechanisms of transmission for representative bunyaviruses that are human pathogens

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
Generic image for table
TABLE 4

CE serogroup viruses

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
Generic image for table
TABLE 5

Clinical and laboratory features of Hantaan virus-associated HFRS and HCPS

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43
Generic image for table
TABLE 6

Hemodynamic summary at clinical nadir of eight HCPS patients with shock

Citation: Mertz G. 2009. : Bunyaviruses, Phleboviruses, Nairoviruses, and Hantaviruses, p 977-1007. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815981.ch43

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