Evaluation of Human-to-Human Transmission of Monkeypox from Infected Patients to Health Care Workers

Fleischauer, Aaron; Kile, James C.; Davidson, M.; Fischer, Marc; Karem, Kevin L.; Teclaw, Robert; Messersmith, Hans; Pontones, Pamela; Beard, Bradley; Braden, Zachary; Cono, Joanne; Sejvar, James J.; Khan, Ali S.; Damon, Inger K.; Kuehnert, Matthew J.

doi:10.1086/427805

Cited by 115 publications

(110 citation statements)

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“…Forty-seven cases of human MPXV infection (confirmed and probable cases; J. Cono, personal communication) were documented, each stemming from direct or indirect contact with MPXV-infected prairie dogs. There were no instances of human-to-human transmission documented [5,19]. Persons who became infected with MPXV were, however, exposed to ill prairie dogs in different settings and by means of varied types of contact [20].…”

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confidence: 99%

Clinical Manifestations of Human Monkeypox Influenced by Route of Infection

et al. 2006

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confidence: 99%

Clinical Manifestations of Human Monkeypox Influenced by Route of Infection

et al. 2006

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“…The ability to trigger a state of nonresponsiveness represents a unique MHC-independent mechanism for blocking antiviral T cell activation and inflammatory cytokine production and is likely an important attribute involved with viral dissemination in the infected host. Although MPV does not spread efficiently by human-to-human contact (12)(13)(14), it serves as an important model for smallpox (15-18) and shares several key features of pathogenesis. For instance, unlike vaccinia (VV) (19), both VAR and MPV disseminate through their infected hosts mainly by a cell-associated viremia (15,(20)(21)(22)(23).…”

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confidence: 99%

“…Inadvertent importation of this virus into the US in 2003 raised MPV awareness and demonstrated first-hand how global travel can quickly lead to unexpected outbreaks of zoonotic diseases (9)(10)(11). Although MPV does not spread efficiently by human-to-human contact (12)(13)(14), it serves as an important model for smallpox (15)(16)(17)(18) and shares several key features of pathogenesis. For instance, unlike vaccinia (VV) (19), both VAR and MPV disseminate through their infected hosts mainly by a cell-associated viremia (15,(20)(21)(22)(23).…”

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confidence: 99%

Monkeypox virus evades antiviral CD4 ⁺ and CD8 ⁺ T cell responses by suppressing cognate T cell activation

Hammarlund

Dasgupta

Pinilla

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

144

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Monkeypox virus (MPV) is a virulent human pathogen that has gained increased attention because of its potential use as a bioterrorism agent and inadvertent introduction into North America in 2003. The US outbreak also provided an important opportunity to study MPV-specific T cell immunity. Although MPV-specific CD4 ؉ and CD8 ؉ T cells could recognize vaccinia virus (VV)-infected monocytes and produce inflammatory cytokines such as IFN␥ and TNF␣, they were largely incapable of responding to autologous MPV-infected cells. Further analysis revealed that, unlike cowpox virus (CPV), MPV did not interfere with MHC expression or intracellular transport of MHC molecules. Instead, MPV-infected cells were capable of preventing T cell receptor (TcR)-mediated T cell activation in trans. The ability to trigger a state of nonresponsiveness represents a unique MHC-independent mechanism for blocking antiviral T cell activation and inflammatory cytokine production and is likely an important attribute involved with viral dissemination in the infected host. Although MPV does not spread efficiently by human-to-human contact (12)(13)(14), it serves as an important model for smallpox (15-18) and shares several key features of pathogenesis. For instance, unlike vaccinia (VV) (19), both VAR and MPV disseminate through their infected hosts mainly by a cell-associated viremia (15,(20)(21)(22)(23). Moreover, evasion of host immune responses is well documented; VAR infection of previously vaccinated humans and MPV infection of non-human primates can result in infectious virus persisting for prolonged periods of time as an asymptomatic infection in apparently healthy individuals (24-32).The mechanisms underlying these forms of immune evasion are not well understood. Many viruses employ a battery of immune evasion strategies (33-38) and poxviruses in particular are equipped to evade antiviral cytokines, chemokines, and/or antigen presentation (35, 39). We have shown that cowpox virus (CPV) interferes with intracellular transport of MHC class I, a process that correlated with evasion of antiviral CD8 ϩ T cell responses by CPV (40). It was recently demonstrated that CPV open reading frame 203 retains MHC class I in the ER (41), and, because MPV encodes a close homologue of CPV203, we expected to find a similar mechanism of immune evasion by MPV. In contrast, we observed that MPV did not down-regulate MHC class I, but instead used a mechanism of evasion that inhibited CD4 ϩ and CD8 ϩ T cell activation after cognate interactions with MPV-infected cells. This mechanism of abrogating local T cell responses may avoid systemic immune suppression, while at the same time protecting the viral reservoir from immune surveillance. Identification of the factor or factors involved with MPV-induced T cell inhibition could prove useful for developing new biologics aimed at preventing or alleviating T cell-mediated diseases (42, 43). Results Antiviral CD4 ؉ and CD8 ؉ T Cells Recognize VV-Infected Monocytes butNot MPV-Infected Monocytes. Several human HLA-bindi...

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“…The preponderance of occupationally acquired cases was unique to Wisconsin during this outbreak. Among other involved states, 1 veterinarian from Indiana had a suspected case, and cases occurred in 2 employees of distributor 1 ( 7 , 21 , 22 ). …”

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confidence: 99%