Nonfatal paralysis, induced by the attenuated Pasteur strain of rabies virus, is characterised by local and irreversible flaccid paralysis of the inoculated limbs. We characterised the spread and localisation of virus in the CNS of infected mice, determined the nature of cell injury and examined the role of the immune response. Data indicate that infection of BALB/c mice induced paralysis in 60% of infected mice, the others recovering without sequelae. In both groups of mice, virus was detected in restricted sub-populations of neurons from the brain and spinal cord, and intensity of the neuropathology correlated with levels of rabies RNA and apoptotic infected neurons. However, apoptosis of neurons and paralysis were not due to a direct deleterious effect of the virus, but induced by a T-dependent immune response, as evidenced by their absence in nude mice. Paralysed and asymptomatic mice developed a similar rabies virus-specific IgG2a antibody response, thus excluding the role of any modification of the humoral immune response. In contrast, three events were critically associated with the development of neurological symptoms: the amount of virus in the CNS, the level of apoptosis in both infected neurons and uninfected surrounding cells and the progressive parenchymal infiltration of CD4 + and CD8 + T cells at the site of infection. These data suggest that during nonfatal rabies infection, the levels of viral replication and primary degeneration of infected neurons by apoptosis could be responsible for the infiltration of T lymphocytes capable of inducing secondary degeneration of neural cells. Journal of NeuroVirology (2000) 6, 359 ‐ 372.

/pdf/induction-of-apoptosis-43uf9wgap5.pdf

induction of apoptosis

• Bats are hosts to a range of pathogens, some of which are known to infect and cause disease in humans and domestic animals. Human activities that increase exposure to bats will likely increase the opportunity for these infections to spill over from bats to humans in the future. • Understanding the impacts of anthropogenic changes on infection dynamics within bat populations is necessary to predict and prevent human infections of bat origin. However, this initially requires understanding both bat populations and the dynamics of infections within them. • We propose that a combination of field and laboratory studies are needed to create data-driven mathematical models to elucidate aspects of bat ecology that are most critical to the dynamics of emerging bat viruses.

/pdf/ecology-of-zoonotic-infectious-diseases-in-bats-current-1hfpgrycqw.pdf

Ecology of zoonotic infectious diseases in bats: current knowledge and future directions

Bats are natural reservoirs for the majority of lyssaviruses globally, and are unique among mammals in having exceptional sociality and longevity. Given these facets, and the recognized status of bats as reservoirs for rabies viruses (RABVs) in the Americas, individual bats may experience repeated exposure to RABV during their lifetime. Nevertheless, little information exists with regard to within-host infection dynamics and the role of immunological memory that may result from abortive RABV infection in bats. In this study, a cohort of big brown bats (Eptesicus fuscus) was infected intramuscularly in the left and right masseter muscles with varying doses [10−0.1–104.9 median mouse intracerebral lethal doses (MICLD50)] of an E. fuscus RABV variant isolated from a naturally infected big brown bat. Surviving bats were infected a second time at 175 days post-(primary) infection with a dose (103.9–104.9 MICLD50) of the same RABV variant. Surviving bats were infected a third time at either 175 or 305 days post-(secondary) infection with a dose (104.9 MICLD50) of the same RABV variant. When correcting for dose, similar mortality was observed following primary and secondary infection, but reduced mortality was observed following the third and last RABV challenge, despite infection with a high viral dose. Inducible RABV-neutralizing antibody titres post-infection were ephemeral among infected individuals, and dropped below levels of detection in several bats between subsequent infections. These results suggest that long-term repeated infection of bats may confer significant immunological memory and reduced susceptibility to RABV infection.

/pdf/host-immunity-to-repeated-rabies-virus-infection-in-big-34rv8r8p9y.pdf

Host immunity to repeated rabies virus infection in big brown bats

Localization and immunological characterization of antigenic domains of the rabies virus internal N and NS proteins.

Nonfatal paralysis, induced by the attenuated Pasteur strain of rabies virus, is characterised by local and irreversible flaccid paralysis of the inoculated limbs. We characterised the spread and l...

Abortive rabies virus central nervous infection is controlled by T lymphocyte local recruitment and induction of apoptosis

When adult mice were injected by the footpad route with the attenuated rabies virus ERA/BHK, serum- and brain-associated antibody and interferon were produced, nonspecific cytotoxic cells and virus-specific cytolytic T cells in the spleen were activated, and a nonlethal infection of the central nervous system occurred. Cyclophosphamide treatment of these animals 1 day after virus infection suppressed antibody formation and induction of cytolytic T cells and resulted in a lethal infection. Virus injection into athymic mice also produced lethal infections. This indicated the importance of the T-cell response in survival but did not allow the response of cytolytic T cells to be distinguished from that of helper T cells. because cyclophosphamide has a longer-lasting effect on B cells than on T cells, the resulting mortality when virus is injected at intervals after cyclophosphamide treatment can be used to distinguish the importance of each of these cells in viral clearance. Although delay of rabies virus ERA/BHK injection until 3 days after cyclophosphamide treatment resulted in induction of a strong cytolytic T-cell response and reduced mortality, the mortality could be further reduced by delaying virus infection until the B-cell response had recovered. This indicated that both humoral and cellular immune components were vital for survival in this model.

Mouse model for abortive rabies infection of the central nervous system.

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Mouse model for abortive rabies infection of the central nervous system.