As with inflammations of the conjunctiva, bacterial infection of the cornea is much less common than viral infection.
However, most of these systems are still much less efficient than viral vectors, especially for in vivo gene delivery.
Although a very large number of formulations exist, nonviral gene delivery (transfection) remains much less efficient than viral gene delivery (transduction) and this remains a barrier to its wider use.
Therefore, understanding the involvement of host factors in virus infection may facilitate the discovery of potential drug candidates because host factors undergo much less mutagenic pressure than viral proteins and may have a universal function during different virus infections.
Thus, the ability to isolate replicating virus in cell culture from postmortem materials was much less sensitive than detection of viral RNA by qRT-PCR.
The molecular mechanisms of bacterial host specificity are much less understood than those of viral pathogens, in part due to the complexity of the molecular composition and cellular structure of bacterial cells.
To date, we have yet to identify functions for all the major gene products, much less grasp their implications for the viral life cycle and pathogenic mechanisms.
If you see a true image of the dress, it is hard to imagine how anyone could ever perceive it as white and gold; however, the viral image is much less clear.
While the consequences of viral oncogenes and infection-related inflammation for tumorigenesis have been extensively studied, the impact of tumour-associated inflammation on viral infection is much less understood.
On the other hand, microbial metagenomes, which followed closely behind the first viral metagenomes, were much less mysterious with <20%% of sequences not matching anything in the databases (Dinsdale et al. 2008).
