The Scientist Image of the Day: Hijacked Immune Cell
"An HIV-infected dendritic cell shoots out thin projections called filopodia (red) with virus particles (white) at their ends"
Interpretation of abstract (PLOS, Pathogens, Aggarwal, et al, 2012):
Viruses are so great at infection and replication due to their ability to navigate hostile environments on their way to infect other cells. 
To navigate the hostile environment, many viruses are able to form actin-rich bridges that reach out and tether to other targets for infection.
Imaging HIV-infected dendritic cells has shown viruses hijacking the dendritic cell’s own actin/membrane network. The hijacking of the dendritic cell’s actin/membrane network is one of the most efficient forms of HIV spread.
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The virus spreads (aka, viral egress) by forming and coupling to viral microspikes (aka, filopodia) within these dendritic cells.  >90% of the microspikes (or filopodia) have immature HIV on their tips, extending 10-20 µm.
Live imaging show that these HIV spikes routinely rotate and pivot at their base and shoot out HIV virus particles (aka, virions) at a rate of ~µm/sec. Using this method to shoot out HIV virus particles leads to up to 800 dendritic cells to immune cell (CD4 T cell) contacts per hour, with some of the infected cells culminating in multiple HIV microspikes tethering together and converging to envelope the CD4 T cell membrane with budding HIV particles.
Forming the long viral spikes depended on the presence of a group of proteins called formin diaphanous 2 (Diaph2). Diaph2 is responsible for the actin being able to form chains and polymerize to form the actin-rich membrane bridge. Formation of the long viral spikes were not dependent on Arp2/3 filopodial pathway. This is significant because the Arp2/3 pathway is often associated with actin polymerization that is toxic and causes disease.
The authors then manipulated HIV Nef and reduced HIV transfer 25x just by reducing the number of viral spikes. The correlation between reduction of viral spikes with the reduction of HIV transfer supports the assertion that the potency of HIV transfer and infection directly depended on how many viral spikes there were.
Thus these observations showed how HIV corrupts the cell interactions between the dendritic cell and CD4 T cell by physically embedding at the ends of the long dendritic cell spiky filopodial networks.

The Scientist Image of the Day: Hijacked Immune Cell

"An HIV-infected dendritic cell shoots out thin projections called filopodia (red) with virus particles (white) at their ends"

Interpretation of abstract (PLOS, Pathogens, Aggarwal, et al, 2012):

Viruses are so great at infection and replication due to their ability to navigate hostile environments on their way to infect other cells.

To navigate the hostile environment, many viruses are able to form actin-rich bridges that reach out and tether to other targets for infection.

Imaging HIV-infected dendritic cells has shown viruses hijacking the dendritic cell’s own actin/membrane network. The hijacking of the dendritic cell’s actin/membrane network is one of the most efficient forms of HIV spread.

The virus spreads (aka, viral egress) by forming and coupling to viral microspikes (aka, filopodia) within these dendritic cells.  >90% of the microspikes (or filopodia) have immature HIV on their tips, extending 10-20 µm.

Live imaging show that these HIV spikes routinely rotate and pivot at their base and shoot out HIV virus particles (aka, virions) at a rate of ~µm/sec. Using this method to shoot out HIV virus particles leads to up to 800 dendritic cells to immune cell (CD4 T cell) contacts per hour, with some of the infected cells culminating in multiple HIV microspikes tethering together and converging to envelope the CD4 T cell membrane with budding HIV particles.

Forming the long viral spikes depended on the presence of a group of proteins called formin diaphanous 2 (Diaph2). Diaph2 is responsible for the actin being able to form chains and polymerize to form the actin-rich membrane bridge. Formation of the long viral spikes were not dependent on Arp2/3 filopodial pathway. This is significant because the Arp2/3 pathway is often associated with actin polymerization that is toxic and causes disease.

The authors then manipulated HIV Nef and reduced HIV transfer 25x just by reducing the number of viral spikes. The correlation between reduction of viral spikes with the reduction of HIV transfer supports the assertion that the potency of HIV transfer and infection directly depended on how many viral spikes there were.

Thus these observations showed how HIV corrupts the cell interactions between the dendritic cell and CD4 T cell by physically embedding at the ends of the long dendritic cell spiky filopodial networks.