Variation in resistance to herpes simplex virus type 1 of oligodendrocytes derived from inbred strains of mice

Thomas, Eva; Lau, Anthony; Kim, Seung Up; Osborne, David; Kastrukoff, Lorne F.

doi:10.1099/0022-1317-72-9-2051

Cited by 18 publications

(12 citation statements)

References 18 publications

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“…The differences are statistically significant (Table 2). Previous studies have attributed differences in mouse strain susceptibility to the extent of glial infection with HSV-1 [33,41,62,63] while other studies have reported differences in resistance to HSV-1to be mediated directly by glial cells [31,64,65]. A similar hierarchical order was previously identified for number and size of demyelinating lesions developing in the same strains of mice [34].…”

Section: Discussionsupporting

confidence: 53%

“…In many but not all mouse strains, this is followed by the development of 'focal' areas of antigen positive neuronal and non-neuronal cells that result from the replication of virus in neurons, degeneration of infected cells, release of virus [53-56], and subsequent infection of surrounding glia [57-59]. The hierarchical order of number and size of 'focal' areas reflects mouse strain differences in resistance of glia to HSV-1 [33,41,64,65]. An immune response clears 'focal' areas of viral antigen positive cells from the CNS but results in the development of demyelinating lesions [42].…”

Section: Discussionmentioning

confidence: 99%

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The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

2012

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BackgroundMice infected with HSV-1 can develop lethal encephalitis or virus induced CNS demyelination. Multiple factors affect outcome including route of infection, virus and mouse strain. When infected with a sub-lethal dose of HSV-1 strain 2 via the oral mucosa, susceptible SJL/J, A/J, and PL/J mice develop demyelinating lesions throughout the brain. In contrast, lesions are restricted to the brainstem (BST) in moderately resistant BALB/c mice and are absent in resistant BL/6 mice. The reasons for the strain differences are unknown.MethodsIn this study, we combine histology, immunohistochemistry, and in-situ hybridization to investigate the relationship between virus and the development of lesions during the early stage (< 24 days PI) of demyelination in different strains of mice.ResultsInitially, viral DNA and antigen positive cells appear sequentially in non-contiguous areas throughout the brains of BALB/c, SJL/J, A/J, and PL/J mice but are restricted to an area of the BST of BL/6 mice. In SJL/J, A/J, and PL/J mice, this is followed by the development of 'focal' areas of virus infected neuronal and non-neuronal cells throughout the brain. The 'focal' areas follow a hierarchical order and co-localize with developing demyelinating lesions. When antigen is cleared, viral DNA positive cells can remain in areas of demyelination; consistent with a latent infection. In contrast, 'focal' areas are restricted to the BST of BALB/c mice and do not occur in BL/6 mice.ConclusionsThe results of this study indicate that susceptible mouse strains, infected with HSV-1 via the oral mucosa, develop CNS demyelination during the first 24 days PI in several stages. These include: the initial spread of virus and infection of cells in non-contiguous areas throughout the brain, the development of 'focal' areas of virus infected neuronal and non-neuronal cells, the co-localization of 'focal' areas with developing demyelinating lesions, and latent infection in a number of the lesions. In contrast, the limited demyelination that develops in BALB/c and the lack of demyelination in BL/6 mice correlates with the limited or lack of 'focal' areas of virus infected neuronal and non-neuronal cells in these two strains.

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Section: Discussionsupporting

confidence: 53%

Section: Discussionmentioning

confidence: 99%

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

2012

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“…A clear consensus that resolves this question never emerged in the literature. Some reports indicated that C57BL/6 mouse cells are far less permissive for HSV-1 replication than BALB/c mouse cells (1,3,59). Others concluded that C57BL/6 mouse cells and BALB/c mouse cells are equally permissive for HSV-1 replication (13,30).…”

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confidence: 99%

Re-Evaluating Natural Resistance to Herpes Simplex Virus Type 1

Halford

Balliet

Gebhardt

2004

J Virol

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It is often stated that individuals of a species can differ significantly in their innate resistance to infection with herpes simplex virus type 1 (HSV-1). Three decades ago Lopez reported that C57BL/6 mice could survive a 5,000-fold-higher inoculum of HSV-1 given intraperitoneally than mice of the A or BALB/c strain (Nature 258:152-153, 1975). Susceptible strains of mice died of encephalitis-like symptoms, suggesting that viral spread to the central nervous system was the cause of death. Although Lopez's study documented that C57BL/6 mice were resistant to the development of HSV-1 encephalitis and mortality, the resistance of C57BL/6 mice to other steps of the HSV-1 infection process was not assessed. The results of the present study extend these observations to clarify the difference between resistance to (i) HSV-1 pathogenesis, (ii) HSV-1 replication, (iii) HSV-1 spread, and (iv) the establishment of latent HSV-1 infection. Although C57BL/6 mice are more resistant to HSV-1 pathogenesis than BALB/c mice, the results of the present study establish that HSV-1 enters, replicates, spreads, and establishes latent infections with virtually identical efficiencies in C57BL/6 and BALB/c mice. These observations raise questions about the validity of the inference that differences in natural resistance are relevant in explaining what differentiates humans with recurrent herpetic disease from the vast majority of asymptomatic carriers of HSV-1 and HSV-2.

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“…Structural cells, as defined by Collier et al (1983), are nonimmune host cells that normally support the replication of HSV‐1. Differences in resistance to HSV‐1 in primary cultures of OL are murine strain‐dependent (Kastrukoff et al, 1987, 1989) and determined subsequent to viral adsorption but prior to the expression of immediate early viral antigens (Thomas et al, 1991, 1997). Preliminary results from this study indicate that similar to experimental animals, differences in resistance to HSV‐1 can be identified in primary cultures of human oligodendrocytes (HOLs) and are donor‐dependent.…”

Section: Primary Oligodendrocyte Cultures Derived From Different Humamentioning

confidence: 99%

“…Using HOL derived from the six donors, viral production studies were performed as previously described (Thomas et al, 1991). In brief, cells were infected with HSV‐1 at different multiplicities of infection (MOIs).…”

Section: Primary Oligodendrocyte Cultures Derived From Different Humamentioning

confidence: 99%

Oligodendrocytes from human donors differ in resistance to herpes simplex virus 1 (HSV‐1)

Kastrukoff

Kim

2002

Glia

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Primary cultures of human oligodendrocytes (HOLs) were established from six different donors. Differences in resistance to infection with herpes simplex virus 1 (HSV-1) were determined between the primary cultures of HOL in tissue culture infective dose 50 (TCID 50 ), indirect immunofluoresence (IF), and serial electron microscopy (EM) studies. Virus production at different multiplicities of infection (MOIs) indicated that differences in HSV-1 replication were statistically significant and MOIdependent. Overall, virus yield from the HOL cultures infected at an MOI of 1 increased up to 6 days postinfection (PI); no additional enhancement occurred at 7 days PI. However, differences in the replication capacity of the six HOL cultures observed at 5 days PI persisted at 6 and 7 days PI. When taken together, the results of these investigations indicate that, similar to experimental animals, resistance to HSV-1 differs between primary cultures of HOL and is donor-dependent. The results also raise the possibility that similar to experimental animals, resistance to HSV-1, mediated at the level of HOL, may be genetically determined. Furthermore, permissive infections of primary cultures of HOL were established with HSV-1 over a wide range of MOIs, similar to results obtained with viral infection of primary murine oligodendrocytes, but neither latent nor abortive infections of HOL were induced in vitro, even at very low MOIs. Resistance to HSV-1, mediated by glial cells, is a nonimmune mechanism that may influence the development of acute CNS infection in man as well as individual susceptibility to this virus. GLIA 38: 87-92, 2002.

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Variation in resistance to herpes simplex virus type 1 of oligodendrocytes derived from inbred strains of mice

Cited by 18 publications

References 18 publications

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

The effect of mouse strain on herpes simplex virus type 1 (HSV-1) infection of the central nervous system (CNS)

Re-Evaluating Natural Resistance to Herpes Simplex Virus Type 1

Oligodendrocytes from human donors differ in resistance to herpes simplex virus 1 (HSV‐1)

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