Optical sensing offers an attractive option for detection of surface biopotentials in human subjects where electromagnetically noisy environments exist or safety requirements dictate a high degree of galvanic isolation. Such circumstances may be found in modern magnetic resonance imaging systems for example. The low signal amplitude and high source impedance of typical biopotentials have made optical transduction an uncommon sensing approach. We propose a solution consisting of an electro-optic phase modulator as a transducer, coupled to a vertical-cavity surface-emitting laser and the self-mixing signal detected via a photodiode. This configuration is physically evaluated with respect to synthesized surface electrocardiographic (EKG) signals of varying amplitudes and using differing optical feedback regimes. Optically detected EKG signals using strong optical feedback show the feasibility of this approach and indicate directions for optimization of the electro-optic transducer for improved signal-to-noise ratios. This may provide a new means of biopotential detection suited for environments characterized by harsh electromagnetic interference.
HIV-1 transmission via sexual exposure is an inefficient process. When transmission does occur, newly infected individuals are colonized by the descendants of either a single virion or a very small number of establishing virions. These transmitted founder (TF) viruses are more interferon (IFN)-resistant than chronic control (CC) viruses present 6 months after transmission. To identify the specific molecular defences that make CC viruses more susceptible to the IFN-induced 'antiviral state', we established a single pair of fluorescent TF and CC viruses and used arrayed interferon-stimulated gene (ISG) expression screening to identify candidate antiviral effectors. However, we observed a relatively uniform ISG resistance of transmitted HIV-1, and this directed us to investigate possible underlying mechanisms. Simple simulations, where we varied a single parameter, illustrated that reduced growth rate could possibly underly apparent interferon sensitivity. To examine this possibility, we closely monitored in vitro propagation of a model TF/CC pair (closely matched in replicative fitness) over a targeted range of IFN concentrations. Fitting standard four-parameter logistic growth models, in which experimental variables were regressed against growth rate and carrying capacity, to our in vitro growth curves, further highlighted that small differences in replicative growth rates could recapitulate our in vitro observations. We reasoned that if growth rate underlies apparent interferon resistance, transmitted HIV-1 would be similarly resistant to any growth rate inhibitor. Accordingly, we show that two transmitted founder HIV-1 viruses are relatively resistant to antiretroviral drugs, while their matched chronic control viruses were more sensitive. We propose that, when present, the apparent IFN resistance of transmitted HIV-1 could possibly be explained by enhanced replicative fitness, as opposed to specific resistance to individual IFN-induced defences. However, further work is required to establish how generalisable this mechanism of relative IFN resistance might be.