Accession Number : AD1009277


Title :   Depletion of Alveolar Macrophages Does Not Prevent Hantavirus Disease Pathogenesis in Golden Syrian Hamsters


Descriptive Note : Journal Article


Corporate Author : USAMRIID Frederick United States


Personal Author(s) : Hooper,Jay W ; Hammerbeck,Christopher D ; Brocato,Rebecca L ; Bell,Todd M ; Schellhase,Christopher W ; Mraz,Steven R ; Queen,Laurie A


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/1009277.pdf


Report Date : 20 May 2016


Pagination or Media Count : 42


Abstract : Andes virus (ANDV) is associated with a lethal vascular leak syndrome in humans termed hantavirus pulmonary syndrome (HPS). The mechanism for the massive vascular leakage associated with HPS is poorly understood, however dysregulation of components of the immune response is often suggested as a possible cause. Alveolar macrophages are found in the alveoli of the lung and represent the first line of defense to many airborne pathogens. To determine whether alveolar macrophages play a role in HPS pathogenesis, alveolar macrophages were depleted in an adult rodent model of HPS that closely resembles human HPS. Syrian hamsters were treated, intratracheally, with clodronate-encapsulated liposomes or control liposomes and were then challenged with ANDV. Treatment with clodronate-encapsulated liposomes resulted in significant reduction in alveolar macrophages but depletion did not prevent pathogenesis or prolong disease. Depletion also did not significantly reduce the amount of virus in the lung of ANDV-infected hamsters but altered neutrophil recruitment, MIP-1 and MIP-2 chemokine expression and VEGF levels in hamster BAL early after intranasal challenge. These data demonstrate that alveolar macrophages may play a limited protective role early after exposure to aerosolized ANDV, but do not directly contribute to hantavirus disease pathogenesis in the hamster model of HPS.


Descriptors :   macrophages , alveoli , Pathogenesis , Hantaan virus , Liposomes , lung diseases , Hamsters


Distribution Statement : APPROVED FOR PUBLIC RELEASE