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Virus ganggang dapat melompat ke sel mamalia
Date:
October 21, 2015
Source:
University of Nebraska-Lincoln
Summary:
Penelitian baru memberikan bukti langsung pertama bahwa virus ganggang - menginfeksi dapat menyerang dan berpotensi mereplikasi ke dalam beberapa sel mamalia . Ini mengikuti sebuah studi 2014 yang menemukan tanda-tanda chlorovirus di cairan tenggorokan peserta manusia .
.............. Dikenal sebagai Acanthocystis turfacea chlorella virus 1 , atau - ATCV 1 , patogen ini adalah yang di antara kelas chloroviruses lama diyakini tinggal hanya di ganggang hijau . Pemikiran yang berubah dengan studi 2014 dari Johns Hopkins University dan UNL yang ditemukannya urutan gen menyerupai dari ATCV - 1 di cairan tenggorokan peserta manusia....more .
Algae virus can
jump to mammalian cells
Verdict still out on whether virus causes slower cognition
Date:
October 21, 2015
Source:
University of Nebraska-Lincoln
Summary:
New research provides first direct evidence that an algae-infecting virus
can invade and potentially replicate within some mammalian cells. It follows up
a 2014 study that found signs of a chlorovirus in throat swabs of human
participants.
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New research led by the University of Nebraska-Lincoln has provided the
first direct evidence that an algae-infecting virus can invade and potentially
replicate within some mammalian cells.
Known as Acanthocystis turfacea chlorella virus 1, or ATCV-1, the pathogen
is among a class of chloroviruses long believed to take up residence only in
green algae. That thinking changed with a 2014 study from Johns Hopkins
University and UNL that found gene sequences resembling those of ATCV-1 in
throat swabs of human participants.
The new study, published in the Journal of Virology, introduced
ATCV-1 to macrophage cells that serve critical functions in the immune
responses of mice, humans and other mammals. By tagging the virus with
fluorescent dye and assembling three-dimensional images of mouse cells, the
authors determined that ATCV-1 successfully infiltrated them.
The authors also measured a three-fold increase in ATCV-1 within 24 hours
of introducing the virus. The relatively modest spike nevertheless suggests
that ATCV-1 can replicate within the macrophage cells, according to co-author
David Dunigan.
Though a few studies have documented viruses jumping from one biological
kingdom to another, chloroviruses were previously thought to have a limited
"host range" that stopped well short of the animal kingdom, Dunigan
said.
"A few years ago, no one I know would have made a prediction like
this," said Dunigan, research professor of plant pathology and member of
the Nebraska Center for Virology. "You probably would've been laughed out
of the room. But we are now in the middle of something that is so very
interesting."
The macrophage cells underwent multiple changes characteristic of those
breached by a virus, Dunigan said. These changes eventually included a form of
programmed death that virologists consider an innate "scorched earth"
defense against the spread of viruses, which require living cells to survive
and replicate.
Before dying, the cells exhibited multiple signs of stress that tentatively
support links to mild cognitive impairments first reported in the 2014 paper,
available at http://go.unl.edu/rfuo. The new study measured a post-viral rise in interleukin 6, a cellular
protein that previous research has linked with diminished spatial learning and
certain neurological diseases. The authors also reported an increase in nitric
oxide, an important signaling molecule that has been associated with memory
impairments when produced in excess.
The 2014 investigation, which was initially designed to test the cognitive
functioning of human participants, found that those with the ATCV-1 DNA
performed slightly worse on measures of visual processing and visual motor
speed. Mice inoculated with the virus showed similar deficits in memory and
attention while navigating mazes. The 2014 paper further suggested that ATCV-1
altered the expression of more than 1,000 genes in the rodent hippocampus, an
area of the brain tied to memory and spatial navigation.
The new study's authors are continuing their collaboration with Johns Hopkins
in the hope of ultimately confirming whether and how the virus contributes to
any cognitive deficits suggested by the initial studies.
"It is still unclear whether the factors induced by the cell-based
virus challenge could also be induced in the whole animal, and whether the
induced factors cause cognitive impairments in the animal or the human,"
said co-author Tom Petro, professor of microbiology and immunology at the
University of Nebraska Medical Center.
Dunigan said he and his colleagues are also searching for other cellular
responses to ATCV-1 while investigating how these responses might drive
systemic changes in mice.
"These are pretty big, unexplored questions," Dunigan said.
"There are so many very basic virological questions that we can and want
to ask."
Story Source:
The above post is reprinted from materials provided byUniversity of Nebraska-Lincoln. Note: Materials may be edited for content and length.
Journal Reference:
1. Thomas M. Petro, Irina V. Agarkova, You Zhou, Robert H. Yolken, James L.
Van Etten, David D. Dunigan. Response of mammalian macrophages to challenge
with theChlorovirusATCV-1. Journal of Virology, 2015;
JVI.01254-15 DOI: 10.1128/JVI.01254-15