Improvise, Adapt, Overcome: Dynamic Resiliency Against Unknown Attack Vectors in Microgrid Cybersecurity Games

Cyber-physical microgrids are vulnerable to rootkit attacks that manipulate system dynamics to create instabilities in the network. Rootkits tend to hide their access level within microgrid system components to launch sudden attacks that prey on the slow response time of defenders to manipulate system trajectory. This problem can be formulated as a multi-stage, non-cooperative, zero-sum game with the attacker and the defender modeled as opposing players. To solve the game, this paper proposes a deep reinforcement learning-based strategy that dynamically identifies rootkit access levels and isolates incoming manipulations by incorporating changes in the defense plan. A major advantage of the proposed strategy is its ability to establish resiliency without altering the physical transmission/distribution network topology, thereby diminishing potential instability issues. The paper also presents several simulation results and case studies to demonstrate the operating mechanism and robustness of the proposed strategy

Digital Twins for Moving Target Defense Validation in AC Microgrids

Cyber-physical microgrids are vulnerable to stealth attacks that can degrade their stability and operability by performing low-magnitude manipulations in a coordinated manner. This paper formulates the interactions between CSAs and microgrid defenders as a non-cooperative, zero-sum game. Additionally, it presents a hybrid Moving Target Defense (MTD) strategy for distributed microgrids that can dynamically alter local control gains to achieve resiliency against Coordinated Stealth Attacks (CSAs). The proposed strategy reduces the success probability of attack(s) by making system dynamics less predictable. The framework also identifies and removes malicious injections by modifying secondary control weights assigned to them. The manipulated signals are reconstructed using an Artificial Neural Network (ANN)-based Digital Twin (DT) to preserve stability. To guarantee additional immunity against instability arising from gain alterations, MTD decisions are also validated (via utility and best response computations) using the DT before actual implementation. The DT is also used to find the minimum perturbation that defenders must achieve to invalidate an attacker's knowledge effectively.Comment: IEEE Energy Conversion Congress and Expo (ECCE) 202

Lost at Sea: Assessment and Evaluation of Rootkit Attacks on Shipboard Microgrids

Increased dependence of the maritime industry on information and communication networks has made shipboard power systems vulnerable to stealthy cyber-attacks. One such attack variant, called rootkit, can leverage system knowledge to hide its presence and allow remotely located malware handlers to gain complete control of infected subsystems. This paper presents a comprehensive evaluation of the threat landscape imposed by such attack variants on Medium Voltage DC (MVDC) shipboard microgrids, including a discussion of their impact on the overall maritime sector in general, and provides several simulation results to demonstrate the same. It also analyzes and presents the actions of possible defense mechanisms, with specific emphasis on evasion, deception, and detection frameworks, that will help ship operators and maritime cybersecurity professionals protect their systems from such attacks.Comment: 2023 IEEE Electric Ship Technologies Symposium (ESTS

HIV-1 Nef induces a Rab11-dependent routing of endocytosed immune costimulatory proteins CD80 and CD86 to the Golgi

The Nef protein of HIV-1 removes the immune costimulatory proteins CD80 and CD86 from the cell surface by a unique clathrin- and dynamin-independent, actin-based endocytic pathway that deploys coupled activation of c-src and Rac. In this study, we show that, similar to major histocompatibility complex class I (MHCI), Nef subsequently reroutes CD80 and CD86 to the Golgi region. However, not only are CD80/CD86 internalized by a different mechanism from MHCI but also the vesicular pathway of Golgi delivery for CD80/CD86 is distinct from that employed for MHCI. While MHCI passes through early endosomal and sorting compartments marked by Rab5/early embryonic antigen 1 and ADP ribosylation factor 6, respectively, CD80 and CD86 enter endocytic vesicles that do not acquire conventional early endosomal markers but remain accessible to fluid probes. Rather than being delivered to preexisting Rab11-positive recycling compartments, these vesicles recruit Rab11 de novo. Rab11 activity is also necessary for the delivery of CD80/CD86 in these transitional vesicles to the Golgi region. These data reveal an unusual pathway of endocytic vesicular traffic to the Golgi and its recruitment in a viral immune evasion strategy

Differential Regulation of Two Arms of mTORC1 Pathway Fine-Tunes Global Protein Synthesis in Resting B Lymphocytes

Protein synthesis is tightly regulated by both gene-specific and global mechanisms to match the metabolic and proliferative demands of the cell. While the regulation of global protein synthesis in response to mitogen or stress signals is relatively well understood in multiple experimental systems, how different cell types fine-tune their basal protein synthesis rate is not known. In a previous study, we showed that resting B and T lymphocytes exhibit dramatic differences in their metabolic profile, with implications for their post-activation function. Here, we show that resting B cells, despite being quiescent, exhibit increased protein synthesis in vivo as well as ex vivo. The increased protein synthesis in B cells is driven by mTORC1, which exhibits an intermediate level of activation in these cells when compared with resting T cells and activated B cells. A comparative analysis of the transcriptome and translatome of these cells indicates that the genes encoding the MHC Class II molecules and their chaperone CD74 are highly translated in B cells. These data suggest that the translatome of B cells shows enrichment for genes associated with antigen processing and presentation. Even though the B cells exhibit higher mTORC1 levels, they prevent the translational activation of TOP mRNAs, which are mostly constituted by ribosomal proteins and other translation factors, by upregulating 4EBP1 levels. This mechanism may keep the protein synthesis machinery under check while enabling higher levels of translation in B cells

HIV-1 Nef promotes endocytosis of cell surface MHC class II molecules via a constitutive pathway

HIV-1 Nef has been reported to disrupt MHC class II (MHCII)-mediated Ag presentation by a dual strategy that comprises a reduction in cell surface levels of peptide-loaded mature MHCII molecules and a up-regulation of immature MHCII molecules. We show that Nef achieves relocation of MHCII away from the cell surface in monocytic cells by both delaying its transport to the cell surface and by accelerating endocytic removal of cell surface MHCII to a lysosomal compartment. Nef-induced MHCII endocytosis is cholesterol-sensitive but clathrin- and dynamin-independent. Internalized MHCII molecules traverse the early endosomal system and colocalize with pinocytic cargo before reaching lysosomes. Nef-triggered MHCII endocytosis requires Rab5 activity and lyst function, whereas lysosomal trafficking of internalized MHCII molecules requires Rab7 activity. We further show that a similar pathway can remove peptide-MHCII complexes from the surface of monocytic cells not expressing Nef. Our data suggest that Nef uses mechanisms involved in normal MHCII recycling and turnover to mediate the delivery of cell surface MHCII to a lysosomal destination. Thus, Nef-mediated endocytosis of MHCII provides a novel perspective on the regulation of normal MHCII trafficking